Create an account and get 3 free clips per day.
Chapters
Hepatocellular Carcinoma, Hepatitis B | Microwave Ablation (US-Guided) | 57 | Female
Hepatocellular Carcinoma, Hepatitis B | Microwave Ablation (US-Guided) | 57 | Female
2016ablateablatingaxialcentimetercoronalechogenichepaticlesionlesionsplaneSIRtumorultrasoundvisualize
VICI Stent Trial Update
VICI Stent Trial Update
acuteBoston ScientificchronicdefinitionsdifferencesDVTendpointfeasibilityinclusioning Stent / Venovo (Bard Medical) - Venous Stent System / Abre (Medtronic) - Venous Self-Exping Stent SystemivusnitinolocclusionocclusionspatencypatientspivotalproximalstenttermstherapeuticthrombotictrialsvenousVenous Stent SystemViciZilver Vena (Cook Medical) - Venous Self-Exp
Summary Of Thermal Ablation RCTs
Summary Of Thermal Ablation RCTs
ablationanteriorClosure SystemcollectedcomparingendovenousEVAEVLTexaminefrequencylaserligationMedtronicMOCAolleoutcomeoutcomespaucityproximalqualityradioactiverctsrecurrencereviewsRFAsaphenoussclerotherapystrippingsurgerysystematictherapeuticthermalThermal AblationtrialsUGFSVenaSealvenousversus
Surveillance Protocol And Reinterventions After F/B/EVAR
Surveillance Protocol And Reinterventions After F/B/EVAR
aneurysmangiographicaorticarteryBbranchbranchedcatheterizationcatheterizedceliaccommoncommon iliacembolizationembolizedendoleakendoleaksevarFfenestratedfenestrationFEVARgastricgrafthepatichypogastriciiiciliacimplantleftleft renalmayomicrocatheternidusOnyx EmbolizationparaplegiapreoperativeproximalreinterventionreinterventionsrenalrepairreperfusionscanstentStent graftsuperselectivesurgicalTEVARtherapeuticthoracicthoracoabdominaltreatedtypeType II Endoleak with aneurysm growth of 1.5 cmVeithvisceral
New Developments In Access Site Closure For Small Sheaths; For Large Sheaths
New Developments In Access Site Closure For Small Sheaths; For Large Sheaths
ambulationantegradearteryassessingcalcifiedCardival Medicalcathcath labCelt ACD (Vasorum) - Vascular Closure DeviceclosurecollagencomplicationcomplicationscompressionconsconsecutivedeploymentdevicedevicesdiscembolizationfemoralhemostasismanualminorminutespatientsprosrandomizedrequiringretrogradestainlesssurgicaltherapeutictimetrialVascade VCDvascularVascular Closure Deviceversusvisualize
Cannulation Mapping: How Does It Help The Dialysis Staff
Cannulation Mapping: How Does It Help The Dialysis Staff
AV AccessbloodbuttoncannulatecannulationDialysisdirectiondrawFistulagraftguidancemarkingmedicalneedleneedlespatientsrealrealtimerequiredultrasoundveinvessel
Yakes Type I, IIb, IIIa And IIIb: The Curative Retrograde Vein Approach
Yakes Type I, IIb, IIIa And IIIb: The Curative Retrograde Vein Approach
alcoholaneurysmalarterialarteryavmsclassificationcoilcoilscombinationcureddirectethanolfillinglesionlesionsmultipleneedlenidusoutflowpredominantpunctureretrogradesingletransvenousveinvenousyakes
The Impact Of Distal Drug Migration On Wound Healing After PTAs With DCBs: A Model To Measure Drug Levels In Tissues
The Impact Of Distal Drug Migration On Wound Healing After PTAs With DCBs: A Model To Measure Drug Levels In Tissues
amputationangioplastyarteryballoonballoonsBoston ScientificcalcificationclinicalcoatedcompleteconcentrationdegreedistaldiureticdownstreamdrugendpointshealinglesionslimbnecrosispaclitaxelPaclitaxel-Coated PTA Balloon CatheterpatientpatientsPTAs with DCBRangerrutherfordsalvagestenosisstudytherapeuticwound
Midterm Comparative Results Of CAS With 2 Mesh Covered Stents - The C-Guard (InspireMD) And The Roadsaver (Terumo)
Midterm Comparative Results Of CAS With 2 Mesh Covered Stents - The C-Guard (InspireMD) And The Roadsaver (Terumo)
activityarterycarotidcarotid arterycarotid stentCASCGuard (InspireMD) - Embolic Prevention Stentconventionalembolizationexternalexternal carotidincidenceipsilateralischemiclesionlesionsocclusionpatencypatientplaquereportedrestenosisriskRoadSaverstenosisstentstentsterumoTerumo interventional systemsTherapeutic / Diagnostic
Bailout Rescue Procedures When CEA Is Failing In A Critical Unstable Patient: ICA Stent Or Gore Hybrid Graft Or Standard PTFE Bypass: Indications For Each
Bailout Rescue Procedures When CEA Is Failing In A Critical Unstable Patient: ICA Stent Or Gore Hybrid Graft Or Standard PTFE Bypass: Indications For Each
anastomosisangiogrambailbypasscarotidCarotid bypassCEACFAdurableembolicendarterectomygoregrafthybridHybrid vascular graftinsertedlesionnitinolpatencypatientperioperativeproximalPTAptferestenosisstenosistechniquetransmuralvascular graft
A New System For Treating Prosthetic Arterial And Aortic Graft Infections
A New System For Treating Prosthetic Arterial And Aortic Graft Infections
abdominalanastomosisaneurysmbiofilmcomorbiditydebridementendovascularenterococcusexplantfasterfavorFemoro-femoral PTFE Bypass infectionfoamgraftinfectedinfectioninstillationintracavitarymalemortalitynegativeNPWTobservationalpatientpreservepressureprostheticptferadiologistremovalspecimensurgicaltherapythoracictreatmentvascularwound
Why Are Carotid Stenoses Under- And Over-Estimated By Duplex Ultrasonography: How To Prevent These Problems
Why Are Carotid Stenoses Under- And Over-Estimated By Duplex Ultrasonography: How To Prevent These Problems
arteriovenousbasicallybrachiocephaliccarotidcommoncontralateraldiameterdiscordancedistalexternalFistulainternallowoccludedocclusionproximalrecanalizedrokestenosistighttumorvelocitiesvelocityvessel
How To Tailor Activity Recommendations To Patients After Cervical Artery Dissection
How To Tailor Activity Recommendations To Patients After Cervical Artery Dissection
adventitiaaneurysmalarteryatheroscleroticavoidaxialcarotidcervicalcoronaldissectiondissectionsexerciseextracranialextravasationextremeheartincludingintimalmaximumneckPathophysiologypatientspredictedpseudoaneurysmrecurrentrisksystemicsystolictemporaltraumavalsalvavertebral
Pitfalls Of Percutaneous EVAR (PEVAR) And How To Avoid Them
Pitfalls Of Percutaneous EVAR (PEVAR) And How To Avoid Them
AbbottaccessanesthesiaAngio-Seal (Terumo Medical Corporation) - Closure deviceangiogramangiosealanteriorarteriotomybifurcationboreclampclosuredeployedEndologixevarfailedfailurefemoralgelfoamhemostasislengthmicropunctureobservedoperativePerclose ProGlidepercutaneousPEVARpredictorsprogliderandomizescarringSuture-Mediated Closure (SMC) Systemtechniquetherapeuticveitvenousvessel
Current Management Of Bleeding Hemodialysis Fistulas: Can The Fistula Be Salvaged
Current Management Of Bleeding Hemodialysis Fistulas: Can The Fistula Be Salvaged
accessaneurysmalapproachArtegraftavoidbleedingbovineBovine Carotid Artery Graft (BCA)carotidcentersDialysisemergencyexperiencefatalFistulafistulasflapgraftgraftshemodialysishemorrhageinfectioninterpositionlesionLimberg skin flapnecrosispatencypatientpatientsptfeskinStent graftsubsequentsuturetourniquetulceratedulcerationsvascular
Utility Of Duplex Ultrasound For Hemodialysis Access Volume Flow And Velocity Measurements
Utility Of Duplex Ultrasound For Hemodialysis Access Volume Flow And Velocity Measurements
accessaneurysmalbypassclinicalDialysisdiameterduplexdynamicflowflowsgraftluminalmeasurepatientsrenalsensitivityultrasoundveinvelocityversusvolume
CMS Policy Update On Nonthermal Ablation
CMS Policy Update On Nonthermal Ablation
ablationanteriorClariVeincompressivecontractorcovercoveragedeterminationsfoamincisionincisionsmedicarementionmicrofoamNonthermal ablationOcclusion catheter systemphlebectomyrefluxsaphenoussclerotherapysystematictherapeutictreatmentsVascular Insights IncvcssVenaSeal (Medtronic - closure system) / Varithena (BTG Interventional Medicine - polidocanol injectable foam) / PhotoDerm VascuLight (ESC - laser device) / Veinlase (Fisma - laser device)venous
New Devices For False Lumen Obliteration With TBADs: Indications And Results
New Devices For False Lumen Obliteration With TBADs: Indications And Results
aneurysmangiographyaortaballooningCcentimeterdilatorendograftendovascularEndovascular DevicefenestratedgraftiliacimplantedlumenoccludeoccluderoccludersoccludesremodelingstentStent graftstentstechniqueTEVARtherapeuticthoracicthoracoabdominalVeithy-plugyplug
Algorithms For Managing Steal Syndrome: When Is Banding Appropriate
Algorithms For Managing Steal Syndrome: When Is Banding Appropriate
accessaccommodateanastomosisarterialarterybandingbasicallybrachialchoiceclipsdigitaldistalFistulaflowgangrenegraftinflowligationlowmorbidneuropathypatencypatientspredictablepreservepressuresprostheticpulserestrictionstealunderwentveinvolume
Surgical Results Of Treating Hepatic Hemangioma And Literature Review
Surgical Results Of Treating Hepatic Hemangioma And Literature Review
adenomaasymptomaticbenignbleedbleedingbloodcapillarycavernouscenterdiagnosisdiagnosticdifferentialexperiencehemangiomahermannlivermalignantmortalityMRIperformsurgeonsurgerysymptomaticsymptomsTherapeutic / Diagnostictransplantationtumorsvessels
Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
Surgical vs. Endovascular Management Of Cephalic Arch Syndrome
adjunctsanatomicangioplastyarchballoonballoonsbrachiocephaliccephalicdeploymentfistulasfunctionalgoregraftgraftingInterventionspatencypredictorsprimaryradiocephalicrecurrentstenosesstenosisstentStent graftstentingsuperiorsurgicaltranspositionviabahn
"Acquired" AVMs: More Common Than We Think
acquiredarterialarteriogramarteriovenousavmscoilcollateralsconnectionsDeep vein trombosisduralDVTentityepisodeevarextensiveextremityfemoralFistulahistoryiliacinflammatorylesionlesionsocclusionpelvicpriorstentingstimulationswellingthrombosistreatedtreatmentuterineveinvenouswayne
Routine Use Of Ultrasound To Avoid Complications During Placement Of Tunneled Dialysis Catheters: Analysis Of 2805 Cases
Routine Use Of Ultrasound To Avoid Complications During Placement Of Tunneled Dialysis Catheters: Analysis Of 2805 Cases
angioplastyarteryballoonBalloon angioplastycannulationcathetercentralchronicallycomplicationsDialysisguidancejugularlesionliteraturemechanicaloccludedpatientsperformedplacementportionroutineroutinelystenoticsubsequenttunneledultrasoundunderwentveinwire
4D Ultrasound Evaluation Of AAAs: What Is It; How Can It Help To Predict Growth And Rupture Rates
4D Ultrasound Evaluation Of AAAs: What Is It; How Can It Help To Predict Growth And Rupture Rates
analysisaneurysmassessmentbasedbiomechanicalcontourdatadiagnosticdistalfieldgrowthimagesimaginglimitationslongitudinalmechanicalmergednephrotoxicparametersperformperformedpredictpredictorpropertiesproximalrupturesegmentationstressultrasoundvalidateviewwall
Selective SMA Stenting With F/EVAR: When Indicated, Value, Best Bridging Stent, Technical Tips
Selective SMA Stenting With F/EVAR: When Indicated, Value, Best Bridging Stent, Technical Tips
aneurysmcookdeviceselevatedendograftfenestratedfenestrationsFEVARgraftI-CAST(ZFEN)intensifiermidtermmortalityorthogonalpatientsrenalselectivestenosisstentstentedstentingtherapeutictreatedVBX (ZFEN)VeithvelocitiesvisceralwideZenith Fenestrated graft
Value Of Intraprocedural Completion Cone Beam CT After Standard EVARs And Complex EVARs (F/B/EVARs): What To Do If One Does Not Have The Technology
Value Of Intraprocedural Completion Cone Beam CT After Standard EVARs And Complex EVARs (F/B/EVARs): What To Do If One Does Not Have The Technology
4-Vessel FEVARangiographyaortoiliacarchaxialbeamBEVARbifurcatedcalcificationcatheterizecatheterizedcompletionconecone beamcoronaldetectablediagnosticdilatordissectionDissection FlapendoleakevaluatesevarfemorofenestratedFEVARfindingsfusionGE HealthcareinterventionmesentericocclusionoperativelypositiveproceduresprospectiveproximalradiationRadiocontrast agentrotationalstentstudytechnicalthoracoabdominaltriggeredunnecessaryVisipaque
Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
Improper And Suboptimal Antiplatelet Treatment Casts Doubt On All CAS Trials: What Are The Implications
accessactiveangioplastyantiplateletaspirincarotidCASconvertcrestdatadecreaseembolicendarterectomyenzymeeventsgroininsertintermediatelivermetabolitenormalpackagepatientspeopleplavixpoorrandomizedrapidriskshiftsitestentstentingstentstechnicaltrialsultra
The Biolux Paseo-18 Lux DCB: Advantages And Good Patency Results In Difficult Fempop Lesions
The Biolux Paseo-18 Lux DCB: Advantages And Good Patency Results In Difficult Fempop Lesions
adverseBailoux Passeo18Bailoux Passeo18 ProcedureballoonBiotronikcalcifiedcentimeterclinicalcohortdrivenfreedomglobalhydrophobiclesionlesionspaclitaxelpatencypatientspercentagephaseprimaryrandomizedregardregistriesstentstentedstentingstudysubgroupstasctherapeuticversus
Update On The Value Of Tack Assisted Balloon Angioplasty (TOBA) : Results Of The TOBA II Study
Update On The Value Of Tack Assisted Balloon Angioplasty (TOBA) : Results Of The TOBA II Study
adjudicatedanchoringbailoutclinicaldissecteddissectionDissection repair devicedissectionsefficacyendovascularenrollenrolledfreedomimplantimprovementIntact MedicallengthlesionlesionsnitinolpatencypatientsPOBAprimaryradiopaqueregardrestenoticstenosisstentTack endovascular systemtargettherapeuticvessel
Elevation Or Retunneling For Second Stage Basilic Vein Transposition
Elevation Or Retunneling For Second Stage Basilic Vein Transposition
anastomosisarterialbasiliccomparablecomparedcumulativedatafavoredFistulafistulasgraftsjournalmaturationOne & Two Stage procedurespatenciespatencyprimaryrangeratesstagestagedstratifiedSuperficializationsuperiorTrans-positiontransectiontransposedtranspositiontunnelingvascularveinveinsversus
Can You Predict Venous Severity Based On Reflux Time
Can You Predict Venous Severity Based On Reflux Time
ablatedablationceapclinicalcorrelationdiameterEndovenous Saphenous AblationfillingMixed Venous DiseaseMixed Venous Disease CEAP Class 5patientsplethysmographypoplitealrefluxsaphenousseverityTherapeutic / Diagnosticveinvelocityvenous
Transcript

Hepatitis B, 3.2 centimeter lesion

adjacent to the hepatic vein so I'll just run through the slides, there you can see it there, and you can see it's right next to the middle hepatic vein. So this is one of these cases where there's no real option here. You can do RF if you want but the chances of it working are pretty

low. So it's these kinds of cases for sure where, in terms of options, what you should do, definitely, personally I think microwave is probably the way to go. >> [COUGH]

>> So you can see here very, very nice echogenic lesion, and again this is one of the benefits of ultrasound, if you do a CT and try and visualize this lesion the chance of you actually being able to see it is almost zero.

So if you're not using ultrasound it's important to start using it, learn the technique. The other thing with ultrasound which you don't get with CT or is more difficult with CT is that you have multiple access options with ultrasound because, you're not sitting just in the axial plane [UNKNOWN]

coronal you can use any plane that you want. You can do out of plane ablations, in other words use ultrasound to visualize your lesion and then you can come into that without having your needle implanged as long as you know exactly where you're going.

So you have a lot more options to treat lesions than you do just using CT guidance. I think it's important, if you're not using it definitely to incorporate it into your practice [BLANK_AUDIO]

So here it is. I just wanna see if this video will play, here we go. As you can see the nice big ablation, we used two probes here as well.

Big ablation, good results and the important thing again, when you're doing these cases what you wanna think about is what the aim is, obviously ablating the tumor, what the risks are, damaged to your surrounding structures and the most appropriate technology.

So again for those kinds of lesions I don't think there's an option, you shouldn't be using a radio frequency oblation in that situation cuz the risk of you leaving a tumor behind from from heat sync is significant and the problem is sometimes you only get one bite at the apple and the first one ti is always the easiest. When you have to go in and re ablate a lesion because you've had a

recurrence it can be very very tricky to know exactly where a tumor is, where a treated tumor is and it just becomes more and more difficult as you go on. So the first time you have a shot at it is the best time, anything after that just makes your life more and more difficult.

- Thank you very much. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,

12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end

or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three

now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing

that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,

they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.

The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal

and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients

were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.

That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.

Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known

that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage

for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available

in about a month, thank you.

- Thank you very much for inviting me here again and I'll be talking about thermal ablation RCTs. My coauthor, Michel Perrin from Lyon, in France, the gourmet capital in the world has collected RCTs on operative treatment of CVD since 1990. Today he has 186 collected RCTs

of the which 84 involve thermal ablation. You can find all this data for free in Phlebolymphology.org. Do we need further RCTs? Well systematic reviews and meta-analyses increasingly important in evidence-based medicine. And this development is well-described

by Gurevitch in Nature this year and criticized by Ioannidis two years earlier. Common sense is a good principle when you try to understand meta-analyses. Do most studies point in the same direction?

Is the effect significant? Are the patient-related outcome measures relevant and what happens if you exclude one study? Since 2008, 10 years back, these are the available meta-analyses and the last came from Ireland earlier this year.

It was published in the JVS, endovenous and in fact this is in March. And they found nine RCTs comparing conventional surgery and endovenous therapy with five years or more follow-up that were selected. Primary outcome was recurrence rate.

There is some sole recurrence rate was that there is no significant difference in laser versus surgery, same for radioactive frequency versus surgery and radioactive frequency versus laser. They found an inferiority

of ultrasound guided foam sclerotherapy versus laser and surgery. Their conclusions were that the quality of evidence is poor therefore more trials that are well-powered to examine long-term outcomes are warranted. The new kids on the block,

steam, MOCA, and Venaseal, are not included in the meta-analyses due to lack of more than five years follow-up in their paper. Obsolete RCTs. Endovenous laser in the presented long-term RCTs

were performed by 810-980 nanometer wavelength using a bare fiber. There is a paucity of RCTs comparing open surgery with novel endovenous laser and new RF techniques. Recent criticism against endovenous ablation, is the pendulum swinging towards high ligation

and stripping again? Olle Nelzen from Sweden in an editorial in British Journal of Surgery reconsidering the endovenous revolution, wrote that neovascularization is a dominant finding following high ligation and stripping

but proximal venous stumps and incompetent anterior accessory saphenous veins are the main factor after endovenous ablation. So long-term follow-up suggests that the recurrence rate after endovenous ablation seem to increase over time. A substantial number of patients who have undergone

endovenous ablation will eventually develop symptomatic recurrence requiring repeat therapy. And such scenario would change the equation regarding patient benefit and costs making endovenous ablation less competitive and challenging current guidelines.

So summary of needs for further RCTs. Quality of present RCTs poor in several meta-analyses, no thermal endovenous technique is superior to open surgery, RCTs rapidly obsolete due to change in technology, and more trials that are well-powered to examine long-term outcomes are warranted.

So final point, apparently we need more RCTs to satisfy the quality requirements for clinically important systematic reviews and meta-analyses. And what about the clinical guidelines? Thank you very much.

- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal

and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks

after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.

So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.

That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied

to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience

there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,

or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.

In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted

for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.

This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,

and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak

and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.

Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.

You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,

so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.

And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR

is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program

with CT scan is of paramount importance after these procedures. I thank you very much for your attention.

- I'd like to thank Dr. Veith for this kind invitation and the committee as well. So these are my disclosures, there's none. So for a quick background regarding closure devices. Vascular closure devices have been around

for almost 20 years, various types. Manual compression in most studies have always been shown to be superior to vascular closure devices mainly because there's been no ideal device that's been innovated to be able

to handle all sorts of anatomies, which include calcified vessels, soft plaque, etc. So in this particular talk we wanted to look at to two particular devices. One is the Vascade vascular closure device

made by Cardiva and the other is the CELT arterial closure device made by Vasorum in Ireland. Both these devices are somewhat similar in that they both use a disc. The Vascade has a nitinol disc

as you can see here that's used out here to adhere to the interior common femoral artery wall. And then once tension is applied, a series of steps is involved to deploy the collagen plug

directly on to the artery which then allows it to expand over a period of time. The CELT is similar in that it also uses a stainless steel disc as you can see here. Requires tension up against the interior wall of the common femoral artery.

Nice and tight and then you screw on the top end of the device on to the interior wall of the artery creating a nice little cylinder that compresses both walls of artery. As far as comparability is concerned between the two devices you can see

here that they're both extravascular, one's nitinol, one's stainless steel. One uses a collagen material, the other uses an external clip in a spindle-type fashion. Both require about, anywhere between three to seven minutes of pressure

to essentially stop the tract ooze. But the key differences between the two devices, is the amount of time it takes for patients to ambulate. So the ambulation time is two hours roughly for Vascade, whereas for a CELT device

it's anywhere from being immediate off the table at the cath lab room to about 20 minutes. The data for Vascade was essentially showing the RESPECT trial which I'll summarize here, With 420 patients that was a randomized trial

to other manual compression or the device itself. The mean points of this is that the hemostasis time was about three minutes versus 21 minutes for manual compression. And time to ambulation was about 3.2 hours versus 5.7 hours.

No major complications were encountered. There were 1.1% of minor complications in the Vascade versus 7% in the manual compression arm. This was actually the first trial that showed that a actual closure devices

had better results than manual compression. The main limitations in the trial didn't involved complex femoral anatomy and renal insufficiency patients which were excluded. The CELT ACD trial involved 207 patients that were randomized to CELT or to manual

compression at five centers. Time to hemostasis was anywhere between zero minutes on average versus eight minutes in the manual compression arm. There was one complication assessed at 30 days and that was a distal embolization that occurred

early on after the deployment with a successfully retrieved percutaneously with a snare. So complication rate in this particular trial was 0.7% versus 0% for manual compression. So what are some pros and cons with the Vascade device?

Well you can see the list of pros there. The thing to keep in mind is that it is extravascular, it is absorbable, it's safe, low pain tolerance with this and the restick is definitely possible. As far as the cons are involved.

The conventional bedrest time is anywhere between two to three hours. It is a passive closure device and it can create some scarring when surgical exploration is necessary on surgical dissections.

The key thing also is you can not visualize the plug after deployment. The pros and cons of the CELT ACD device. You can see is the key is the instant definitive closure that's achieved with this particular device, especially in

calcified arteries as well. Very easy to visualize under fluoroscopy and ultrasound. It can be used in both antegrade and retrograde approaches. The key cons are that it's a permanent implant.

So it's like a star closed devised, little piece of stainless steel that sits behind. There's a small learning curve with the device. And of course there's a little bit of discomfort associated with the cinching under the (mumbles) tissue.

So we looked at our own experience with both devices at the Christie Clinic. We looked at Vascade with approximately 300 consecutive patients and we assessed their time to hemostasis, their time to ambulation,

and their time to discharge, as well as the device success and minor and major complications. And the key things to go over here is that the time to hemostasis was about 4.7 minutes for Vascade, at 2.1 hours for ambulation, and roughly an average

of 2.4 hours for discharge. The device success was 99.3% with a minor complication rate of .02% which we have four hematomas and two device failures requiring manual compression. The CELT ACD device we also similarly did

a non-randomized perspective single center trial assessing the same factors and assessing the patients at seven days. We had 400 consecutive patients enrolled. And you can see we did 232 retrograde. We did a little bit something different

with this one, we did we 168 antegrade but we also did direct punctures to the SFA both at the proximal and the mid-segments of the SFA. And the time to hemostasis in this particular situation was 3.8 minutes,

ambulation was 18.3 minutes, and discharge was at 38.4 minutes. We did have two minor complications. One of which was a mal-deployment of the device requiring manual compression. And the second one was a major complication

which was an embolization of the device immediately after deployment which was done successfully snared through an eighth front sheath. So in conclusion both devices are safe and effective and used for both

antegrade and retrograde access. They're definitely comparable when it comes, from the standpoint of both devices (mumbles) manual compression and they're definitely really cost effective in that they definitely do increase the

throughput in the cath lab allowing us to be able to move patients through our cath lab in a relatively quick fashion. Thank you for your attention.

- This is in line with the earlier discussions we have had regarding cannulation and things. I don't have any disclosure with this. Now, Doctor Sher gave me this topic about cannulation mapping, how does it help dialysis staff? I thought I'd probably try to dissect this a little bit by giving a short introduction and try to define

what I'm talking about and try to look into a little bit about who uses this, who cannulates, and what are the critical components required to make the cannulation safe, so on and so forth. And I'll summarize what I am talking about. As we know, for having successful dialysis we need

about 350 to 450 mls of blood going to the machine and this is drawn by putting two needles in a subcutaneous conduit which has got high blood flow, maybe a graft or a fistula. And it requires two needles to get in there, one to pull the blood out to the machine

and second one to push the blood back. So what is cannulation? One can probably say cannulation is the act of insertion of a needle into a vessel to allow blood to be successfully drawn out by the dialyzer pump and returned to the blood vessel.

Who cannulates? Generally if you look in American practice we are talking about technicians cannulating, and technicians, til recently, the basic qualification required to apply for this job was high school diploma. Nowadays some of the units look for MA's and CNA trainings

that that way they have some medical background. But most of the training for cannulation happens on site by senior people who are there and that's the only training people get. Many of the people do not have medical background. So what do they cannulate?

We create all sorts of access. When you talk about fistula we have fistula which are deep, we have fistula which are coiled, we have fistula which are kind of short, we have a fistula long, in the armpit, all over the place. Then we have grafts in our patients.

When they get into problems we try to do all sort of exotic graft like chest wall graft, necklace graft, forearm, upper arm graft, multiple scars. Now obviously, for someone who is got minimum training, doesn't have much medical background, we have to have some sort of a guidance

and that is cannulation mapping. What is cannulation mapping? It is any guidance to facilitate reliable cannulation. And if you think of in terms of guidance we can do it in two ways. One is we can mark and document and communicate.

The other thing is realtime guidance. Realtime guidance can be off site or can be on site. So marking probably should include nature of the conduit. Are you cannulating a graft or a fistula? Those are two different ways of cannulation, 100% different material.

You also need to talk about what are the direction of blood flow. What are the cannulation segments? Where do you cannulate and how deep is the vessel because depth of the vessel determines what angle you use for cannulation,

to be on the safer side. And these instructions should be given to the people who are cannulating. And how do we collect this data? Most of us have access to ultrasound if not we have a lab nearby which has an ultrasound.

Ultrasound can pretty much look into all the parameters including the flow, direction of flow, depth of the vein, size of the vein, cannulation segment, and everything else. We could document it and we could come with form. This is the form I use before sending any

of my patient to dialysis unit before they start cannulating. And this has all the information required for the nurses. We do that. We draw the cannula, we draw the outflow vein pattern, or cannulation segment pattern, and I confirm it

with ultrasound to make sure that if I can draw without using an ultrasound somebody else should be able to find it by clinical exam and I confirm my drawing is right. That way there's no confusion. We draw it on the paper if need be,

send it with the patient. Most of our patients do have cell phones now. We make the patients take the picture with their own cell phone that way they have that documented because this marking is going to go away. And for the marking to stay there for some time

we cover it up with some transparent tegaderm or some sort of a dressing that way when they go to the dialysis they have the marking. They're going with the sheet, with the instruction how to cannulate, where to cannulate, what is the direction of the vein,

how deep it is, maybe you should not use much of an angle, try to keep the needle flat to the skin, so on and so forth. Now, can we do it real time? Real time can be done off site. I have my pediatric nurses who come to my office all the time with the kids

when the first time when I can. I show them with the ultrasound. Any time a cannulator comes to your office and looks with ultrasound, believe me, their whole impression of what is under the skin becomes clearer

because ultrasound shows you what exactly is under the skin there. So, it is a good way of doing it, little bit shy of being real time in the unit. So they can come to you and when they see such things, you try to have results like this.

Here's a button hole which is created not on top of the vein because it's very superficial and you may cannulate, you may infiltrate, but it's created on the side of the vein. And that is only because they had a mental conception of how to do this button hole, or train the button hole,

and it's working pretty well for a long period of time. Now, real time cannulation can be done in the units. There are lot of articles out there giving you how to do it, how to image a vessel, and how to put the needle in. And some people have started writing about it

because many of the units have acquired ultrasounds. Obviously it's kind of based on who's running the unit. And this is not a routine or a norm because most of the companies they don't have funding to get the unit. But you know I was talking to you about being in Japan. When you go to their unit they do have

hand held ultrasound machines and they do categorize their patients as patients who are easy to cannulate, patients who are in between, and patients who are difficult to cannulate. Patients who are difficult to cannulate do use ultrasound for cannulation.

They hardly ever superficialize their vessels. So there are real advantages for using an ultrasound real time. Now, obviously the disadvantage becomes costs associated with it, but I feel a cost saving done by ultrasound by preventing infiltrations,

infiltration related hospitalization, loss of access, need for catheters, so on and so forth by far supersedes the cost in ward in getting one or using one. So just to summarize. Morphology of the access can be very varied.

Existing training pathways for cannulation personnel is inadequate to produce expert cannulators. Any cannulation mapping is valuable to increase cannulation safety and the patient's comfort. Ultrasound is an excellent tool for cannulation mapping. Real time ultrasound is useful

to provide cannulation guidelines and availability of real time ultrasound in dialysis unit is cost saving measure that could significantly impact patient safety and satisfaction. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you very much Mr. Chairman. Thank you Frank, for this kind invitation again to this symposium. This is my disclosure. With the drug coated balloons it is important to minimize the drug loss during the balloon transit during the inflation of the balloon.

Because Paclitaxel has a high degree of cytotoxicity that may induce necrosis and increase inflammation in the distal tissue, and we know that even with the best technique, we can loose 70 - 80% of the drop to the distal circulation,

the inference by different factors between them and the calcification of degree of these blood cells. There are adverse events secondary to drug coated balloons that have been reported recently. In animal molders it has shown that Downstream Vascular Changes are more frequent with

Drug Coated Balloons than with Drug-Eluting Stents. In animal molders it has been also shown that there is no evidence of significant downstream emboli or systemic toxicity with DCB's than with patients with controls. This was a study presented yesterday by (mumbles)

with a very nice and elegant study with a good methodology that shows in animals that there are different concentrations of the drug in distal tissue depending on the balloon that you are using. In this case, the range in balloon (mumbles)

those ones have the lowest concentration in the distal tissue. In clinical experience in this meta-analysis amputations and wound healing rate are lower with this series with controls. But there is controversy because

Complete Index Ulcer Healing is higher in this series than with control patients. But there are lower wound healing index in patients compared with drug-eluting stents. In the debate, (mumbles) and also in the dialux which are clinical trials in diuretic patients with CLI,

there we no issues of safety and no impair of the wounds healing. But, remember the negative result of the IN PACT DEEP trial in which there were more amputation at six months that could be influenced, but in all their factors, the lack of standardized

wound care protocols. (mumbles) has also reported recently good survival to 100% in patient treated with DCB's compared with plain balloons and with lutonic balloons. So in our institution, we did a study with the objective to examine

patient outcomes following the use of the drug-coated balloons in patients with CLI and diuretic patients with Complex Real World lesions undergoing endovascular intervention below-the-knee with the Ranger balloon coated with Paclitaxel.

This is a Two-Center Experience that is headed by the National University of Mexico in 30 patients with strict followup. With symptomatic Rutherford four to six. With the Stenosis and occlusion of infrapopliteal vessels and many degrees of calcification.

It was mandatory for all patients to have Pre-dilation before the use of DCB. We studied some endpoints like efficacy. (mumbles) Limb salvage, sustained clinical improvement, wound healing rate

and technical success and some other endpoints of safety. This is an example of multi level disease in a patient that has to be approached by (mumbles) access with a balloon preparation of the artery before the use of the DCB, and after this, we treated the anterior artery

and even to the arch of the foot. This is the way we follow our patient with ultra sound duplex with an index fibular of no more that 2.4. All patients were diabetic with Rutherford 5-6. 77% have a (mumbles) at the initial of the study.

And as you can see there were longer lesions and with higher degree of calcification and stenosis only in two of them we produced (mumbles). There were bailout stent placements in five patients and we did retrograde access in 43 patients.

Subintimal angioplasty was done in 32 patients, and Complete Index Wound Healing was in 93 of our patients. This is our Limb Salvage 94%. The Patency rate was 96% with this Kaplan Meir analysis. And in some patients we did a determination of Paclitaxel concentration in distal tissue

with the High Pressure Liquid Chromatography method. We only did this in five patients because of the lack of financial support, and technical problems. As you can see in three of them we had Complete Wound Healing.

Only one we had major amputation. This was the patient with the higher concentration of Paclitaxel in the distal tissue, and in one patient, we could not determine the concentration of Paclitaxel. This is the way we do this.

They take the sample of the patient at the moment we do the minor amputation. During day 10 after the angioplasty, we also do a (mumbles) analysis of the patient we have a limb salvage we can see arterial and capillar vessel proliferation and hyperplasia of the

arteriole media layer. But, in those patients that have major amputation even when they have a good sterio-graphic result like in this case, we see more fibrinoid necrosis which is a bad determination. So in conclusion,

angioplasty with the (mumbles) balloon maintain clinical efficacy over time is possible. We didn't see No Downstream clinical important or significant effects and high rates of Limb Salvage in complex CLI patients is possible.

Local toxic effects of paclitaxel and significant drug loss on the way to the lesion are theoretical considerations up to now because there is no biological study that can confirm this. Thank you very much.

- Thank you, chairman. Good afternoon, ladies and gentlemen. I've not this conflict of interest on this topic. So, discussion about double-layer stent has been mainly focused about the incidence of new lesions, chemical lesions after the stenting, and because there are still some issue

about the plaque prolapse, this has still has been reduced in a comparison to conventional stent that's still present. We started our study two years ago to evaluate on two different set of population of a patient who underwent stent, stenting,

to see if there is any different between the result of two stents, Cguard from Inspire, and Roadsaver from Terumo in term of ischemic lesion and if there is a relationship between the activity of the plaque evaluated with the MRI

and new ischemic lesion after the procedure. So, the population was aware of similar what we found, and that there's no difference between the two stent we have had, and new ischemic lesions is, there's a 38%, for a total amount of 34 lesions,

and ipsilateral in 82% of cases. The most part of the lesion appeared at the 24 hours, for the 88.2% of cases, while only the 12% of cases, we have a control at our lesion. According to the DWI, we have seen that

the DWI of the plaque is positive, or there is an activity of the plaque. There's a higher risk of embolization with a high likelihood or a risk of 6.25%. But, in the end, what we learned in the beginning, what there have known,

there's no difference in the treatment of the carotid stenosis with this device, and the plaque activity, when positive at the DWI MR, is a predictive for a higher risk of new ischemic lesions at 24 hours. But, what we are still missing in terms of information,

where something about the patency of the stents at mid-term follow-up, and the destiny of external carotid artery at mid-term follow-up. Alright, we have to say we have an occlusion transitory, occlusion of the semi-carotid artery

immediately after the deployment of the Terumo stent. The ECA recovery completely. But in, what we want to check, what could happen, following the patient in the next year. So, we perform a duplicate ultrasound, at six, at 12, and 24 months after the procedure,

in order to re-evaluate the in-stent restenosis and then, if there was a new external carotid artery stenosis or occlusion. We have made this evaluation according to the criteria of grading of carotid in-stent restenosis proposed on Stroke by professors attache group.

And what we found that we are an incidence of in-stent restenosis of 10%, of five on 50 patient, one at six month and four at one year. And we are 4% of external carotid artery new stenosis. All in two patient, only in the Roadsaver group.

We are three in-stent restenosis for Roadsaver, two in-stent restenosis for Cguard, and external new stenosis only in the Roadsaver group. And this is a case of Roadsaver stent in-stent restenosis of 60% at one year. Two year follow-up,

so we compare what's happening for Cguard and Roadsaver. We see that no relation have been found with the plaque activity or the device. If we check our result, even if this is a small series, we both reported in the literature for the conventional stent,

we've seen that in our personal series, with the 10% of in-stent restenosis, that it's consistent with what's reported for conventional CAS. And the same we found when we compared our result with the result reported for CAS with conventional stent.

So in our personal series, we had not external carotid artery occlusion. We have 4% instance, and for stenosis while with conventional CAS, occlusion of external carotid artery appear in 3.8% of cases.

So, what can we add to our experience now in the incidence, if, I'm sorry, if confirmed by larger count of patient and longer study? We can say that the incidence of in-stent restenosis for this new double-layer stent and the stenosis on the external carotid artery,

if not the different for all, with what reported for conventional stent. Thank you.

- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years

of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).

It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,

it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases

that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it

was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.

And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted

inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted

selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.

In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients

stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.

This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,

and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,

and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

(applause)

- [Nicos] Thanks so much. Good afternoon everybody. I have no disclosures. Getting falsely high velocities because of contralateral tight stenosis or occlusion, our case in one third of the people under this condition, high blood pressure, tumor fed by the carotid, local inflammation, and rarely by arteriovenous fistula or malformation.

Here you see a classic example, the common carotid, on the right side is occluded, also the internal carotid is occluded, and here you're getting really high velocity, it's 340, but if you visually look at the vessel, the vessel is pretty wide open. So it's very easy to see this discordance

between the diameter and the velocity. For occasions like this I'm going to show you with the ultrasound or other techniques, planimetric evaluation and if I don't go in trials, hopefully we can present next year. Another condition is to do the stenosis on the stent.

Typically the error here is if you measure the velocity outside the stent, inside the stent, basically it's different material with elastic vessel, and this can basically bring your ratio higher up. Ideally, when possible, you use the intra-stent ratio and this will give you a more accurate result.

Another mistake that is being done is that you can confuse the external with the internal, particularly also we found out that only one-third of the people internalized the external carotid, but here you should not make this mistake because you can see the branches obviously, but really, statistically speaking, if you take 100

consecutively occluded carotids, by statistical chance 99% of the time or more it will be not be an issue, that's common sense. And of course here I have internalization of the external, let's not confuse there too, but here we don't have any

stenosis, really we have increased velocity of the external because a type three carotid body tumor, let's not confuse this from this issue. Another thing which is a common mistake people say, because the velocity is above the levels we put, you see it's 148 and 47, this will make you with a grand criteria

having a 50% stenosis, but it's also the thing here is just tortuosity, and usually on the outer curve of a vessel or in a tube the velocity is higher. Then it can have also a kink, which can produce the a mild kink like this

on here, it can make the stenosis appear more than 50% when actually the vessel does have a major issue. This he point I want to make with the FMD is consistently chemical gradual shift, because the endostatin velocity is higher

than people having a similar degree of stenosis. Fistula is very rare, some of our over-diligent residents sometimes they can connect the jugular vein with roke last year because of this. Now, falsely low velocities because of proximal stenosis of

the Common Carotid or Brachiocephalic Artery, low blood pressure, low cardiac output, valve stenosis efficiency, stroke, and distal ICA stenosis or occlusion, and ICA recanalization. Here you see in a person with a real tight stenosis, basically the velocity is very low,

you don't have a super high velocity. Here's a person with an occlusion of the Common Carotid, but then the Internal Carotid is open, it flooded vessels from the external to the internal, and that presses a really tight stenosis of the external or the internal, but the velocities are low just because

the Common Carotid is occluded. Here is a phenomenon we did with a university partner in 2011, you see a recanalized Carotid has this kind of diameter, which goes all the way to the brain and a velocity really low but a stenosis really tight. In a person with a Distal dissection, you have low velocity

because basically you have high resistance to outflow and that's why the velocities are low. Here is an occlusion of the Brachiocephalic artery and you see all the phenomena, so earlier like the Common Carotid, same thing with the Takayasu's Arteritis, and one way I want to finish

this slide is what you should do basically when the velocity must reduce: planimetric evaluation. I'll give you the preview of this idea, which is supported by intracarotid triplanar arteriography. If the diameter of the internal isn't two millimeters, then it's 95% possible the value for stenosis,

regardless of the size of the Internal Carotid. So you either use the ICAs, right, then you're for sure a good value, it's a simple measurement independent of everything. Thank you very much.

- Thank you very much. It's an hono ou to the committee for the invitation. So, I'll be discussing activity recommendations for our patients after cervical artery dissection. I have no relevant disclosures.

And extracranial cervical artery dissection is an imaging diagnosis as we know with a variety of presentations. You can see on the far left the intimal flap and double lumen in the left vertebral artery

on both coronal and axial imaging, a pseudoaneurysm of the internal carotid artery, aneurysmal degeneration in an older dissection, and an area of long, smooth narrowing followed by normal artery, and finally a flame-tipped occlusion.

Now, this affects our younger patients with really opposity of atherosclerotic risk factors. So, cervical artery dissection accounts for up to 25% of stroke in patients under the age of 45. And, other than hypertension, it's not associated with any cardiovascular risk factors.

There is a male predominance, although women with dissections seem to present about five years younger. And there is an indication that there may be a systemic ateriopathy contributing to this in our patients, and I'll show you some brief data regarding that.

So, in studies that have looked at vessel redundancy, including loops, coils, and in the video image, an S curve on carotid duplex. Patients with cervical artery dissection have a much higher proportion of these findings, up to three to four times more than

age and sex matched controls. They also have findings on histology of the temporal artery when biopsied. So one study did this and these patients had abnormal capillary formation as well as extravasation of blood cells between the median adventitia

of the superficial temporal artery. And there is an association with FMD and a shared genetic polymorphism indicating that there may be shared pathophysiology for these conditions. But in addition, a lot of patients report minor trauma around the time or event of cervical artery dissection.

So this data from CADISP, and up to 40% of cases had minor trauma related to their dissection, including chiropractic neck manipulation, extreme head movements, or stretching, weight lifting, and sports-related injuries. Thankfully, the majority of patients do very well after

they have a dissection event, but a big area of concern for the patient and their provider is their risk for recurrence. That's highest around the original event, about 2% within the first month, and thereafter, it's stable at 1% per year,

although recurrent pain can linger for many years. So what can we tell our patients in terms of reducing their risk for a recurrent event? Well, most of the methods are around reducing any sort of impulse, stress, or pressure on the arteries, both intrinsically and extrinsically,

including blood pressure control. I advise my patients to avoid heavy lifting, and by that I mean more than 30 pounds, and intense valsalva or isometric exercise. So shown here is a photo of the original World's Strongest Man lifting four

adult-sized males in addition to weights, but there's been studies in the physiology literature with healthy, younger males in their 20s, and they're asked to do a double-leg press, or even arm-curls, and with this exercise and repetitions, they can get mean systolic pressures,

or mean pressures up into the 300s, as well as heart rate into the 170s. I also tell my patients to avoid any chiropractic neck manipulation or deep tissue massage of the neck, as well as high G-force activities like a roller coaster.

There are some case reports of cervical artery dissection related to this. And then finally, what can they do about cardio? A lot of these patients are very anxious, they're concerned about re-incorporating exercise after they've been through something like this,

so I try to give them some kind of guidelines and parameters that they can follow when they re institute exercise, not unlike cardiac rehabilitation. So initially, I tell them "You can do light walking, but if you don't feel well,

or something's hurting, neck pain, headache, don't push it." Thereafter, they can intensify to a heart rate maximum of 70-75% of their maximum predicted heart rate, and that's somewhere between months zero and three, and then afterwards when they're feeling near normal,

I give them an absolute limit of 90% of their maximum predicted heart rate. And I advise all of my patients to avoid extreme exercise like Orange Theory, maybe even extreme cycling classes, marathons, et cetera. Thank you.

- Thank you very much and I would like to thank Dr. Veit for the kind invitation, this is really great meeting. Those are my disclosures. Percutaneous EVAR has been first reported in the late 1990's. However, for many reasons it has not been embraced

by the vascular community, despite the fact that it has been shown that the procedure can be done under local anesthesia and it decreases OR time, time to ambulation, wound complication and length of stay. There are three landmark papers which actually change this trend and make PEVAR more popular.

All of these three papers concluded that failure or observed failure of PEVAR are observed and addressed in the OR which is a key issue. And there was no late failures. Another paper which is really very prominent

is a prospective randomize study that's reported by Endologix and published in 2014. Which revealed that PEVAR closure of the arteriotomy is not inferior to open cut down. Basically, this paper also made it possible for the FDA to approve the device, the ProGlide device,

for closure of large bore arteriotomies, up to 26 in the arterial system and 29 in the venous system. We introduced percutaneous access first policy in our institution 2012. And recently we analyzed our results of 272 elective EVAR performed during the 2012 to 2016.

And we attempted PEVAR in 206 cases. And were successful in 92% of cases. But the question was what happened with the patient that failed PEVAR? And what we found that was significantly higher thrombosis, vessel thrombosis,

as well as blood loss, more than 500 cc in the failed PEVAR group. Similarly, there was longer operative time and post-operative length of stay was significantly longer. However, in this relatively small group of patients who we scheduled for cut-down due to different reasons,

we found that actually there was no difference between the PEVAR and the cut-down, failed PEVAR and cut-down in the terms of blood loss, thrombosis of the vessel, operative time and post-operative length of stay. So what are the predictors of ProGlide failure?

Small vessel calcification, particularly anterior wall calcification, prior cut-down and scarring of the groin, high femoral bifurcation and use of large bore sheaths, as well as morbid obesity. So how can we avoid failures?

I think that the key issue is access. So we recommend that all access now or we demand from our fellow that when we're going to do the operation with them, cut-down during fluoroscopy on the ultra-sound guidance, using micropuncture kits and access angiogram is actually mandatory.

But what happened when there is a lack of hemostasis once we've deployed two PEVARs? Number one, we try not to use more than three ProGlide on each side. Once the three ProGlide failed we use the angioseal. There's a new technique that we can have body wire

and deployed angioseal and still have an access. We also developed a technique that we pack the access site routinely with gelfoam and thrombin. And also we use so-called pull and clamp technique, shown here. Basically what it is, we pull the string of the ProGlide

and clamp it on the skin level. This is actually a very very very good technique. So in conclusion, PEVAR first approach strategy successful in more than 90% of cases, reduced operative time and postoperative length of stay, the failure occurred more commonly when the PEVAR

was completed outside of IFU, and there was no differences in outcome between failed PEVAR and planned femoral cut-down. Thank you.

- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop

and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about

the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,

the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience

in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come

from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which

they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.

So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.

Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.

Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.

But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap

and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.

When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.

If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis

of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft

or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at

how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure

they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE

as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition

a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use

the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with

a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.

Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned

even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,

well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.

If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula

but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.

Prevention is vital and educating our patients and dialysis centers is key. Thank you.

- So this was born out of the idea that there were some patients who come to us with a positive physical exam or problems on dialysis, bleeding after dialysis, high pressures, low flows, that still have normal fistulograms. And as our nephrology colleagues teach us, each time you give a patient some contrast,

you lose some renal function that they maintain, even those patients who are on dialysis have some renal function. And constantly giving them contrasts is generally not a good thing. So we all know that intimal hyperplasia

is the Achilles Heel of dialysis access. We try to do surveillance. Debbie talked about the one minute check and how effective dialysis is. Has good sensitivity on good specificity, but poor sensitivity in determining

dialysis access problems. There are other measured parameters that we can use which have good specificity and a little better sensitivity. But what about ultrasound? What about using ultrasound as a surveillance tool and how do you use it?

Well the DOQI guidelines, the first ones, not the ones that are coming out, I guess, talked about different ways to assess dialysis access. And one of the ways, obviously, was using duplex ultrasound. Access flows that are less than 600

or if they're high flows with greater than 20% decrease, those are things that should stimulate a further look for clinical stenosis. Even the IACAVAL recommendations do, indeed, talk about volume flow and looking at volume flow. So is it volume flow?

Or is it velocity that we want to look at? And in our hands, it's been a very, very challenging subject and those of you who are involved with Vasculef probably have the same thing. Medicare has determined that dialysis shouldn't, dialysis access should not be surveilled with ultrasound.

It's not medically necessary unless you have a specific reason for looking at the dialysis access, you can't simply surveil as much as you do a bypass graft despite the work that's been done with bypass graft showing how intervening on a failing graft

is better than a failed graft. There was a good meta-analysis done a few years ago looking at all these different studies that have come out, looking at velocity versus volume. And in that study, their conclusion, unfortunately, is that it's really difficult to tell you

what you should use as volume versus velocity. The problem with it is this. And it becomes, and I'll show you towards the end, is a simple math problem that calculating volume flows is simply a product of area and velocity. In terms of area, you have to measure the luminal diameter,

and then you take the luminal diameter, and you calculate the area. Well area, we all remember, is pi r squared. So you now divide the diameter in half and then you square it. So I don't know about you,

but whenever I measure something on the ultrasound machine, you know, I could be off by half a millimeter, or even a millimeter. Well when you're talking about a four, five millimeter vessel, that's 10, 20% difference.

Now you square that and you've got a big difference. So it's important to use the longitudinal view when you're measuring diameter. Always measure it if you can. It peaks distally, and obviously try to measure it in an non-aneurysmal area.

Well, you know, I'm sure your patients are the same as mine. This is what some of our patients look like. Not many, but this is kind of an exaggerated point to make the point. There's tortuosity, there's aneurysms,

and the vein diameter varies along the length of the access that presents challenges. Well what about velocity? Well, I think most of us realize that a velocity between 100 to 300 is probably normal. A velocity that's over 500, in this case is about 600,

is probably abnormal, and probably represents a stenosis, right? Well, wait a minute, not necessarily. You have to look at the fluid dynamic model of this, and look at what we're actually looking at. This flow is very different.

This is not like any, not like a bypass graft. You've got flow taking a 180 degree turn at the anastomosis. Isn't that going to give you increased turbulence? Isn't that going to change your velocity? Some of the flow dynamic principles that are important

to understand when looking at this is that the difference between plug and laminar flow. Plug flow is where every bit is moving at the same velocity, the same point from top to bottom. But we know that's not true. We know that within vessels, for the most part,

we have laminar flow. So flow along the walls tends to be a little bit less than flow in the middle. That presents a problem for us. And then when you get into the aneurysmal section, and you've got turbulent flow,

then all bets are off there. So it's important, when you take your sample volume, you take it across the whole vessel. And then you get into something called the Time-Averaged mean velocity which is a term that's used in the ultrasound literature.

But it basically talks about making sure that your sample volume is as wide as it can be. You have to make sure that your angle is as normal in 60 degrees because once you get above 60 degrees, you start to throw it off.

So again, you've now got angulation of the anastomosis and then the compliance of a vein and a graft differs from the artery. So we use the two, we multiply it, and we come up with the volume flow. Well, people have said you should use a straight segment

of the graft to measure that. Five centimeters away from the anastomosis, or any major branches. Some people have actually suggested just using a brachial artery to assess that. Well the problems in dialysis access

is there are branches and bifurcations, pseudoaneurysms, occlusions, et cetera. I don't know about you, but if I have a AV graft, I can measure the volume flow at different points in the graft to get different numbers. How is that possible?

Absolutely not possible. You've got a tube with no branches that should be the same at the beginning and the end of the graft. But again, it becomes a simple math problem. The area that you're calculating is half the diameter squared.

So there's definitely measurement area with the electronic calipers. The velocity, you've got sampling error, you've got the anatomy, which distorts velocity, and then you've got the angle with which it is taken. So when you start multiplying all this,

you've got a big reason for variations in flow. We looked at 82 patients in our study. We double blinded it. We used a fistulagram as the gold standard. The duplex flow was calculated at three different spots. Duplex velocity at five different spots.

And then the diameters and aneurysmal areas were noted. This is the data. And basically, what it showed, was something totally non-significant. We really couldn't say anything about it. It was a trend toward lower flows,

how the gradients (mumbles) anastomosis, but nothing we could say. So as you all know, you can't really prove the null hypothesis. I'm not here to tell you to use one or use the other, I don't think that volume flow is something that

we can use as a predictor of success or failure, really. So in conclusion, what we found, is that Debbie Brow is right. Clinical examinations probably still the best technique. Look for abnormalities on dialysis. What's the use of duplex ultrasound in dialysis or patients?

And I think we're going to hear that in the next speaker. But probably good for vein mapping. Definitely good for vein mapping, arterial inflow, and maybe predicting maturation. Thank you very much.

- [Narrator] So my assignment is, CMS policy update on non-thermal ablation techniques, and as most of you know, there is not one National CMS policy, so there are a variety of local cover determinations or policies that we're going to look at. I may bore you for a couple minutes

but I found a surprise at the end. So I went to the website, CMS website, and looked up varicose vein LCDs and these seven came up, interestingly Novitas, everybody's favorite, didn't come. So I looked at separately, we're going to look at all these as well.

And here is Novitas, Novitas and their previous LCD had no mention of non-thermal techniques, but in this proposed LCD, which has a lot of people up in arms, they say that the non-thermal techniques are experimental, investigational, and unproven,

and therefore will not be covered. This is next LCDs, this is two from Medicare contractor Noridian, they go on to talk about sclerotherapy and foam sclerotherapy, but they are not going to cover it. And somewhat bizarrely these codes in red here,

which are for Venaseal and Verithena, are listed as indications for RF or laser ablation, which kind of shows you they don't know what they're talking about. And there is no mention of MOCA or Claravein. Wisconsin Physicians Services and other MAC contractor,

and I looked at their LCD, there is no mention of non-thermal techniques. Next up is First Coast Service Options, with these jurisdictions over here on the right. And they get down to the C-classification, VCSS score, and talk about compressive therapy and conservative therapy.

They do mention Clarivein or MOCA. However, they state that it does not meet the Medicare necessity for coverage, and so they won't. And there's absolutely no mention of Verithena or Venaseal in their LCD. Palmetto GBA is another contractor,

with these jurisdictions on the right, and they actually discuss and approve Varithena, microfoam sclerotherapy. They discuss it here in their LCD, they have some restrictions that the physician needs to be competent and experienced with Varithena,

and ultrasound, there is no mention of Clarivein or Venaseal in their LCD. And these are also the folks that tell us how to do stab phlebectomy with 2 mm incisions and a crochet hook. So don't use a 3 mm incision and a hemostat,

it'd probably get denied. Next is CGS Administrators, and this busy slide, they go on to talk about sclerotherapy quite a bit, and all these in the main body, what they are not going to cover for sclerotherapy. They mention that foam sclerotherapy

is basically the same as liquid sclerotherapy, and therefore will not cover it, and again no mention of other treatments of non-thermal techniques. Which brings us to the last LCD, which is National Government Services,

and amazingly they state that the accepted treatments for eliminating reflux and the great saphenous anterior accessory, and small saphenous vein, include RFA, laser, polidocanol, Venaseal, and Verithena. And even more interestingly, they use their Rationale for Determination for MOCA.

The amount and consistency of the data, in addition to the two recent systematic reviews and the strong recommendation of the American Venous Forum, have convinced NGS that Medicare coverage is met. And for PEM, Varithena, the combination of RCTs, meta-analyses, systematic reviews,

the strong recommendation of the AVF, and endorsements from the SVS, ACP, SCAI, and SIR, have convinced them that coverage is appropriate. And the same for Venaseal, same thing. This is craziness. On one Medicare hand,

you have Novitas saying that, treatment is experimental and unproven, and they won't cover it. And on the other Medicare hand, you have this contractor that says, based on the recommendations of the experts,

that it's appropriate, and will be covered. And this is the reason why we need a National Coverage Determination. So, to find out what your policy is, you have to go to the website, you have to find out who your provider is,

or contractor, and see what the policy cause it differs depending upon where you are. Thank you for your attention.

- Thank you (mumbles) and thank you Dr. Veith for the kind invitation to participate in this amazing meeting. This is work from Hamburg mainly and we all know that TEVAR is the first endovascular treatment of choice but a third of our patients will fail to remodel and that's due to the consistent and persistent

flow in the false lumen over the re-entrance in the thoracoabdominal aorta. Therefore it makes sense to try to divide the compartments of the aorta and try to occlude flow in the false lumen and this can be tried by several means as coils, plug and glue

but also iliac occluders but they all have the disadvantage that they don't get over 24 mm which is usually not enough to occlude the false lumen. Therefore my colleague, Tilo Kolbel came up with this first idea with using

a pre-bulged stent graft at the midportion which after ballooning disrupts the dissection membrane and opposes the outer wall and therefore occludes backflow into the aneurysm sac in the thoracic segment, but the most convenient

and easy to use tool is the candy-plug which is a double tapered endograft with a midsegment that is 18 mm and once implanted in the false lumen at the level of the supraceliac aorta it occludes the backflow in the false lumen in the thoracic aorta

and we have seen very good remodeling with this approach. You see here a patient who completely regressed over three years and it also answers the question how it behaves with respect to true and false lumen. The true lumen always wins and because once

the false lumen thrombosis and the true lumen also has the arterial pressure it does prevail. These are the results from Hamburg with an experience of 33 patients and also the international experience with the CMD device that has been implanted in more than 20 cases worldwide

and we can see that the interprocedural technical success is extremely high, 100% with no irrelevant complications and also a complete false lumen that is very high, up to 95%. This is the evolvement of the candy-plug

over the years. It started as a surgeon modified graft just making a tie around one of the stents evolving to a CMD and then the last generation candy-plug II that came up 2017 and the difference, or the new aspect

of the candy-plug II is that it has a sleeve inside and therefore you can retrieve the dilator without having to put another central occluder or a plug in the central portion. Therefore when the dilator is outside of the sleeve the backflow occludes the sleeve

and you don't have to do anything else, but you have to be careful not to dislodge the whole stent graft while retrieving the dilator. This is a case of a patient with post (mumbles) dissection.

This is the technique of how we do it, access to the false lumen and deployment of the stent graft in the false lumen next to the true lumen stent graft being conscious of the fact that you don't go below the edge of the true lumen endograft

to avoid (mumbles) and the final angiography showing no backflow in the aneurysm. This is how we measure and it's quite simple. You just need about a centimeter in the supraceliac aorta where it's not massively dilated and then you just do an over-sizing

in the false lumen according to the Croissant technique as Ste-phan He-lo-sa has described by 10 to 30% and what is very important is that in these cases you don't burn any bridges. You can still have a good treatment

of the thoracic component and come back and do the fenestrated branch repair for the thoracoabdominal aorta if you have to. Thank you very much for your attention. (applause)

- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed

is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome

is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement

and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.

So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.

We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy

which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures

that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.

As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.

So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,

and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.

So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.

It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,

'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula

and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.

It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically

a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.

Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal

vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.

Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding

the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody

who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test

confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,

so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,

although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.

It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get

a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.

And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,

immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.

We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.

So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,

and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.

DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,

when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%

in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.

They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.

If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.

And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.

If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.

The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis

greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,

including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,

the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,

at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft

rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.

We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.

And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.

And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.

Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,

cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered

earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Narrator] Okay, very interesting hypothesis.

- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide

and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter

is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues

that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement

of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side

and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,

then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,

coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,

and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques

with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation

of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.

We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go

so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side

or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.

Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.

On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded

and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.

Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.

Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,

despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients

to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,

and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,

and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.

- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,

it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.

And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication

what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies

to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging

that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,

with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures

to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit

in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is

based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,

and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.

Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system

that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress

and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform

a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.

I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient

before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.

But we hope to present on that more solid data next year. Thank you very much.

- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.

You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience

the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,

as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.

If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.

We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.

Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.

No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time

of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities

and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice

In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases

due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.

We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.

So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed

with multi-institution trial and longer follow-up

- [Speaker] Good morning everybody thanks for attending the session and again thanks for the invitation. These are my disclosures. I will start by illustrating one of the cases where we did not use cone beam CT and evidently there were numerous mistakes on this

from planning to conducting the case. But we didn't notice on the completion of geography in folding of the stent which was very clearly apparent on the first CT scan. Fortunately we were able to revise this and have a good outcome.

That certainly led to unnecessary re intervention. We have looked at over the years our usage of fusion and cone beam and as you can see for fenestrated cases, pretty much this was incorporated routinely in our practice in the later part of the experience.

When we looked at the study of the patients that didn't have the cone beam CT, eight percent had re intervention from a technical problem that was potentially avoidable and on the group that had cone beam CT, eight percent had findings that were immediately revised with no

re interventions that were potentially avoidable. This is the concept of our GE Discovery System with fusion and the ability to do cone beam CT. Our protocol includes two spins. First we do one without contrast to evaluate calcification and other artifacts and also to generate a rotational DSA.

That can be also analyzed on axial coronal with a 3D reconstruction. Which essentially evaluates the segment that was treated, whether it was the arch on the arch branch on a thoracoabdominal or aortoiliac segment.

We have recently conducted a prospective non-randomized study that was presented at the Vascular Annual Meeting by Dr. Tenario. On this study, we looked at findings that were to prompt an immediate re intervention that is either a type one

or a type 3 endoleak or a severe stent compression. This was a prospective study so we could be judged for being over cautious but 25% of the procedures had 52 positive findings. That included most often a stent compression or kink in 17% a type one or three endoleak

in 9% or a minority with dissection and thrombus. Evidently not all this triggered an immediate revision, but 16% we elected to treat because we thought it was potentially going to lead to a bad complication. Here is a case where on the completion selective angiography

of the SMA this apparently looks very good without any lesions. However on the cone beam CT, you can see on the axial view a dissection flap. We immediately re catheterized the SMA. You note here there is abrupt stop of the SMA.

We were unable to catheterize this with a blood wire. That led to a conversion where after proximal control we opened the SMA. There was a dissection flap which was excised using balloon control in the stent as proximal control.

We placed a patch and we got a good result with no complications. But considerably, if this patient was missed in the OR and found hours after the procedure he would have major mesenteric ischemia. On this study, DSA alone would have missed

positive findings in 34 of the 43 procedures, or 79% of the procedures that had positive findings including 21 of the 28 that triggered immediate revision. There were only four procedures. 2% had additional findings on the CT

that were not detectable by either the DSA or cone beam CT. And those were usually in the femoro puncture. For example one of the patients had a femoro puncture occlusion that was noted immediately by the femoro pulse.

The DSA accounts for approximately 20% of our total radiation dose. However, it allows us to eliminate CT post operatively which was done as part of this protocol, and therefore the amount of radiation exposed for the patient

was decreased by 55-65% in addition to the cost containment of avoiding this first CT scan in our prospective protocol. In conclusion cone beam CT has allowed immediate assessment to identify technical problems that are not easily detectable by DSA.

These immediate revisions may avoid unnecessary re interventions. What to do if you don't have it? You have to be aware that this procedure that are complex, they are bound to have some technical mistakes. You have to have incredible attention to detail.

Evidently the procedures can be done, but you would have to have a low threshold to revise. For example a flared stent if the dilator of the relic gleam or the dilator of you bifurcated devise encroach the stent during parts of the procedure. Thank you very much.

(audience applauding)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Yeah, thank you very much. We all know that DCBs are kind of a workhorse right now for SFA-PA disease but when it comes, this has been proven randomized controlled studies, but when it comes to real world patients this might not have been included in the randomized conduit study and therefore

these registries are very available. And I present on this BIOLUX P-III study [Unintelligible] the standard versus the non-standard sub-group. This is just a quick overlook about the Passeo-18 Lux DCB it's an O-18 platform, has three micrograms

[Unintelligible] Paclitaxel on the balloon The excipient is a BTHC and this is an hydrophobic excipient and the sizes available are from two to seven millimeter in diameter and four 80 and 100 millimeter in length. This is the overlooks about the Passeo-18 Lux

they are out there, we have from phase one to phase three studies, randomized controlled and global registries. 1,600 patients including in this clinical program. With regard to the full cohort at 12 month we have now 878 patients available, you see with regard to the clinical characteristics

heavy smokers... a high percentage of smokers, high percentage of diabetes, more than 40% of CLI, 76% calcified lesions, the lesion length was around 9 centimeter and one-third of the patients had TASC C or D lesions. This is a higher payload stenting rate

this is not surprising with this complex cohort about 20% and with that the primary patency of the full cohort at 12 months is 84.3% and the freedom from clinical driven TLR is 93.5%. So this is the overlook of the full cohort at 12 months. With regard to the different subgroups you see

you have a consistent freedom from clinical driven TLR primary patency and freedom from major target limb amputation throughout all the subgroups. And I just now want to highlight the bail-out stented versus the DCB only group because this follows the concept of the so-called leave, at least leave less behind

as possible, this so-called spot-stenting concept. Out of this 878 patients we had 715 treated with a DCB only and in the bail-out stent group we had 163 patients. The patients in the bail-out stented group had a longer lesion length... 11 compared to 8 centimeters

in the DCB only group. With regard to all the others correctors there was no difference besides TASC C and D lesions there had been a higher percentage of TASC C and D lesions in the bail-out stented group than in the DCB only group.

We did the same vessel prep for both arms and with that we had the freedom from clinical driven TLR in the bail-out stented group of 92.8 compared to 92.2% in DCB only group. Primary patency was a little bit lower but freedom from a major adverse event

at 12 months was the same. When we bring this into context to other randomized, other real-world data out there freedom from clinical driven TLR in comparison to the In.Pact global stented group is the same as well as in the Lutonix global stented group.

With regard to freedom from major adverse event we can only refer to the In.Pact global stented group which is the same. So just let me conclude the Passeo-18 Biolux P-III study continues to show consistent, clinical performance of the Passeo-18 Lux Drug Coated Balloon

throughout all subgroups. There is no difference in clinical performance between DCB only versus payload stented even for the bail-out stented group had more complex lesions and the results of the Biolux P-III payload stenting subgroups are in line with the results

of current Global registries stented subgroups. Thank you very much.

- So I have the honor to provide you with the 12-month result of the TOBA II trial. I guess we all confirmed that this action is the primary mechanism of angioplasty. We all know that lesions of dissection have a TLR rate of 3.5 times higher than lesions without dissection.

The current tools for dissection repair, these are stents. They have limitations, really a large metal load left behind causing inflammation. This is leading to in-stent restenosis. So the Tack Endovascular System.

It's a delivery system over six French catheter. This is for above the knee with six implants pre-loaded on a single catheter. The Tack implant itself, it has an adaptive sizing, so it adapts to the diameter of the vessel from 2.6 up to 6.0 for SFA and PPA usage.

It's a nitinol implant with gold radiopaque markers for visibility. Has a unique anchoring system, which prevents migration, and a deck which is deployed in six millimeter in length. So with regard to the TOBA II study design,

this was a prospective multi-center single-arm non-blinded study at 33 sites in US and Europe. We enrolled 213 subjects. These were all subjects with post-PTA dissection. So only with a dissection visible on the angiogram, the patients could be enrolled into this study.

We had the usually primary safety end point, primary efficacy end points, which we are familiar from other trials and other studies so far. With regard to the inclusion criteria, I just want to look at this very briefly.

Mainly we had de novo or non-stented restenotic lesions in the SFA P1. If it was a stenosis, the lesion length could be up to 150 millimeter. If it was a total occlusion, the length was up to 10 centimeters.

They had to be the presence of at least one target run of vessel to the foot. They had to be a post residual, post-PTA residual stenosis of lower than 30%, and the presence of at least one dissection Grade A to F. With regard to the key lesion characteristics,

baseline for the different patients, there was not a big difference to other studies out there. The only difference was maybe we had slightly more patients with diabetes. The lesion, the target lesion length, the mean target lesion length was up to 74 millimeters.

We also had patients with calcification, mainly moderate but also some with severe calcification. There were two met the primary end points. The 30-day freedom from major adverse event, and also the primary efficacy end point at 12 months, which was a freedom from clinical driven TLR,

and freedom from core lab adjudicated duplex ultrasound derived binary restenosis. Now, with regard to patency in a patient cohort, where we really had 100% dissected vessel at 100% dissected vessel population, we had primary patency at 12-month of 79.3%

and a freedom clinical driven TLR of 86.5%. There was with regard to dissection severity, we had 369 total dissections we were treating. The number of dissections per subject was 1.8. The mean dissection length was two centimeters. So around 70% of subjects had a dissection of

Grade C or greater before using the Tack. In 92.1% of all dissections, this could be completely resolved with a Tack. With regard to the Tack stability and durability, in total, 871 Tacks have been deployed. So that was a number of 4.1 Tacks per subject.

The bailout stent rate was very low, just one. The freedom from Tack fracture at 12 months, 100%, and there was one minor Tack migration at 12 months with education by the core lab so the Tack was not seen at the same place as six months or 12 months before.

There was significant clinical improvement with Rutherford category improvement in 63%, which improved of up to two classes. There was also an improvement in ABI, walking impairment questionnaire. So just to conclude, TOBA II is a unique trial.

First to enroll 100% dissected vessels. Successfully met the primary efficacy and safety end points, and demonstrated the Tack is an efficient repair system for dissections after POBA or DCB with minimum metal left behind, low radial force, stable and durable design,

and preservation of future treatment options. There was only a very, very low bailout stent rate. This in combination with high patency rate and high freedom from clinical TLR. Thank you very much.

- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations

related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,

and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be

a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation

of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest

as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher

patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.

The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence

that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization

versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,

in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,

one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients

who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored

superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months

for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.

But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear

to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.

Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.

- [Bill] Thank you Vikay. I think this is an interesting topic for many reasons but one of the key ones is that if you look at our health care policies by insurers, this tends to define our practice. So I looked at BlueCross BlueShield's policy and they say that treatment of the GSV or SSV

is medically necessary when there is demonstrated saphenous reflux and I looked for more and there was no more. That's all they said so they must think that reflux a time correlates with venous severity. So is this true?

I think, personally, that there are other things that are involved and that volume is really the key. Time, velocity and the diameter of the vein are likely all part of the process and we all know that obstruction

is also critically important as well and probably the worse patients are those that have both reflux and obstruction. Probably reflux is worse in the deep system but we know that large GSV and SSV patients can develop CEAP four to six symptoms

and do very well with saphenous ablations. And I think this is a nice analogy. I love this guy, it looks like he came off of his lawn chair to help the firefighters out but he's probably not going to do so much with his little garden hose now, is he?

So I think size and velocity do matter. What does the literature tell us? Chris Lattimer and his group have done an elegant set of studies looking at how various parameters correlate to air plethysmography and venous filling times. They did show that there is a correlation

between venous filling time and reflux time. However, other things were probably more correlated such as GSV diameter and reflux velocity. And in this nice study of 300 patients they found that there was a relatively weak correlation between reflux time and clinical severity

and their conclusion was that it was a good parameter to identify reflux but not for quantifying the severity. So here's how we use this clinically in my practice. So you see many patients such as this that have mixed venous disease.

53-year-old female, severe edema. You do her studies and she's got reflux in the deep and the superficial system. So how to we decide if saphenous ablation is going to help this patient or not and correct these symptoms, prevent further ulcerations?

So all reflux is not created equal. The top is a popliteal tracing where the maximum reflux velocity is about five centimeters per second versus the bottom one that's about thirty to forty centimeters per second

so these probably aren't going to behave similarly in when we look at them. So we studied this in 75 patients and reported this back in 2008. We look at the maximum reflux velocity in the popliteal vein to tell if these patients

would improve after we ablated their saphenous or not. We found that this was a significant predictor of both improvement in venous filling index and the venous clinical severity score so we think velocity really does matter. And this is where we're seeing this clinically.

This is a patient that was referred to me for a second opinion concerning whether she would need ablation of her great saphenous vein. And this is the reflux tracing and you can see the scale here is turned up so that this is a measurement of reflux at about two centimeters per second.

This was used to document abnormal reflux and to justify ablation of the saphenous. So I checked one of our tracings. This is what it looks like.

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.