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Degenerative disc disease with Stenosis | Spinal Fusion | MySpine & M.U.S.T | 37 yo Female
Degenerative disc disease with Stenosis | Spinal Fusion | MySpine & M.U.S.T | 37 yo Female
2016chapterdegenerativelumbarMedactaNASSnoindexspinestenosisthoracic
New Developments In The Management Of Thoracic Outlet Syndromes (TOSs): Neurogenic, Venous And Arterial
New Developments In The Management Of Thoracic Outlet Syndromes (TOSs): Neurogenic, Venous And Arterial
inconsistentnetherlandsneurogenicoutcomesoutletpatientsreportingseveritystandardizesurgerytalktextbookthoracic
Aortic Endograft Infection Is A New Epidemic: What Are The Best Treatment Options
Aortic Endograft Infection Is A New Epidemic: What Are The Best Treatment Options
anatomicAorta EndograftaorticcomorbiditiesendograftendograftsendoleakexcisiongraftgraminfectionmortalitymultiplepatientsprostheticstandardizedtherapeuticthoracicZenith/TAG/Medtronic/Endologix
The
The "Spider Graft": A New Hybrid Graft For Treatment Of TAAAs: How Does It Work: Advantages And Results
anastomosesanastomosisantegradeaortaarteriesarteryceliaccenterscompletelydevicedissectiondistalendovascularextracorporealflowgrafthybridiliacintroducedischemialumbarmesentericperformedproximalrenalretroperitonealspinalstentstentedthoracicthoracoabdominalthoraxvisceral
New Developments In Radioactive Sodium Fluoride (18F-FBG) Imaging On PET CT To Predict AAA And TAAA Growth And Rupture
New Developments In Radioactive Sodium Fluoride (18F-FBG) Imaging On PET CT To Predict AAA And TAAA Growth And Rupture
aneurysmaneurysmsaorticarthritisatheroscleroticbiomarkerscalcificationcarotidclinicalcohortcolorcoronarydetectionevaluationgrowthimaginginflammationinflammatoryobservedosseouspatientsperformedplaquepredictrupturesodiumspecificstenosisstudythoracictripleuptake
TEVAR Under Local Anesthesia: How To Do It: Advantages And Limitations
TEVAR Under Local Anesthesia: How To Do It: Advantages And Limitations
anesthesiaaneurysmangulationaorticapproachascendingbloodconsciouscoronarydeployeddevicedischargedejectionendoleakendovasculargrafthemodynamicinnominatepacingpatientpercutaneouspercutaneouslypreventsprocedurepseudoaneurysmrapidrepairstentStent graftstiffTAVRtechniqueTEVARthoracictypicallyvalveventricle
Sandwich Graft Technique For Treating TAAAs: How To Make It Work Even In Urgent Or Ruptured Cases
Sandwich Graft Technique For Treating TAAAs: How To Make It Work Even In Urgent Or Ruptured Cases
a large juxtarenal aneurysmabdominalacuteaneurysmaneurysmsangiogramangioplastyaorticarteryaxillarycarotidcatheterizecatheterizedceliaccentimetercongestivedissectionembolizedendografterectilegraftgraftsiliacsivusleft carotid subclavian bypassleft subclavian artery embolizationlumenluminaloccludedparallelperformedperfusionreasonablerenalrenalssscansegmentstenosisstentssubclavianTEVARtherapeuticthoracicthoracoabdominalType B thoracic dissectionvesselsvisceralwich graft technique
Bare Stent Suprarenal Fixation For EVAR: Is It Harmful Or Beneficial: What Are The Pros And Cons
Bare Stent Suprarenal Fixation For EVAR: Is It Harmful Or Beneficial: What Are The Pros And Cons
aneurysmalaortaaorticbarebifurcatedbifurcationceliaccomponentsdegenerativeembolizationendoleakevarevolutionextensionfenestratedgraftinfrarenalneckocclusionostiumparallelrenalstenosisstentstentingsuprarenalthoracicthoracoabdominaltricks
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
angioplastyanteriorarteriographyarteryballoonclinicalcontralateralcorrelatedDESdopplerdrugdrug elutingDrug eluting stentdysfunctionelutingendovascularerectileevaluationHigh grade bilateral internal pudendal artery stenosisiliacimprovementinternalInternal pudendal artery stentingMedtronicmultifactorialpatientsPOBAprocedurepudendalResolutestenosisstentstentedstentingStenting with a drug-eluting stentsystolictherapeutictreatment
Early Experience With The Gore Endograft For Treating Lesions Of The Ascending Aorta: Advantages And Limitations
Early Experience With The Gore Endograft For Treating Lesions Of The Ascending Aorta: Advantages And Limitations
anesthesiologyangiographicaorticascendingcentersdakedegenerativedevicedevicesdissectionsdistalendovascularexclusionexpandedextenderimagingimplantsinvestigationalneurologicpatientsproximalriskstentTAVRtearthoracicvalvular
TEVAR Under Local Anesthesia: How To Do It: Advantages And Limitations
TEVAR Under Local Anesthesia: How To Do It: Advantages And Limitations
anesthesiaaneurysmangulationaorticapproachascendingbloodconsciouscoronarydeployeddevicedischargedejectionendoleakendovasculargrafthemodynamicinnominatepacingpatientpercutaneouspercutaneouslypreventsprocedurepseudoaneurysmrapidrepairstentStent graftstiffTAVRtechniqueTEVARthoracictypicallyvalveventricle
How TEVAR And EVAR Can Have A Detrimental Effect On The Heart: What Can Be Done About It
How TEVAR And EVAR Can Have A Detrimental Effect On The Heart: What Can Be Done About It
aneurysmsarterialatrialbiomarkerscardiaccardiovasculardiastolicendothelialendovascularevarfavorfollowupgraftincreaseleftmorbiditymortalitymyocardialpatientsperioperativeptfepulseregistryreinterventionsstentstiffnessstudysubendocardialsurvivaltendencyTEVARTherapeutic / Diagnosticthoracictrialsvelocityventricularwave
Value Of A Vascular Surgeon To The Practice Of Other Specialties And To An Institution: How Can Vascular Surgeons Be Adequately Compensated By Institutions For Their Unique And Vital Contributions
Value Of A Vascular Surgeon To The Practice Of Other Specialties And To An Institution: How Can Vascular Surgeons Be Adequately Compensated By Institutions For Their Unique And Vital Contributions
aneurysmcardiaccenterscoworkersenablingendovascularfavorablehealthcarehospitalimpactmarginmedicareorthopedicpatientspayorprofessionalrevenuervusspecialtiesspinestentsurgeonsurgeonssurgeryvascularVeith
Strokes (Clinical And Subclinical) After CAS And Other Interventional Procedures Have Much Greater Cognitive Deficits Than Previously Thought – Even With Full Neurological Recovery: What Are The Implications
Strokes (Clinical And Subclinical) After CAS And Other Interventional Procedures Have Much Greater Cognitive Deficits Than Previously Thought – Even With Full Neurological Recovery: What Are The Implications
aorticcarotidCarotid StentingclinicalCoronar stentdebrisdegenerativeembolicevidencefiltersinterventionallesionsmajorneurocognitiveneurologicobviouspredisposeproceduresprotectionproximalreleasesilkspitestentingstentsstudiesTAVRtrials
Risk Assessment For Thrombosis Prophylaxis In Vascular Surgery - Necessary Or A Nuisance
Risk Assessment For Thrombosis Prophylaxis In Vascular Surgery - Necessary Or A Nuisance
anticoagulantsantiphospholipidantiplateletDVTendovascularfactorsfamilyhistoryincidenceinfrainguinalinpatientintraoperativepatientsperioperativepreoperativeriskscreeningsurgicalthoracicthrombosisvascularvenous
A Novel Front-Cutting Atherectomy Device With Plaque Fragment Aspiration: How Does It Work And Value In Crossing CTOs And Lowering Plaque Burden
A Novel Front-Cutting Atherectomy Device With Plaque Fragment Aspiration: How Does It Work And Value In Crossing CTOs And Lowering Plaque Burden
accomplishedadequateamputationsatherectomycatheterclaudicationdeviceembolicembolizationfollowhybridHybrid AtherectomyimprovementischemialesionslimbpatientsPhillipsPhoenixPhoenix Atherectomy Systemproceduralrotationalrutherfordstenosistherapeuticunplannedutilizes
Delayed vs. Early Intervention (CEA/CAS) In Patients With Carotid Stenosis And Recent Strokes: Patients Should Be Individualized: In What % Is The Stroke Not Due To The Carotid Lesion
Delayed vs. Early Intervention (CEA/CAS) In Patients With Carotid Stenosis And Recent Strokes: Patients Should Be Individualized: In What % Is The Stroke Not Due To The Carotid Lesion
arterycarotidcryptogenicdiagnosedendarterectomyentityintracranialmedicalminorneurologicalpatientsplaquerecurrentriskrisksstenosisstentingstrokessymptomatictherapytreatmenturgent
New Developments In The Management Of Thoracic Outlet Syndromes (TOSs): Neurogenic, Venous And Arterial
New Developments In The Management Of Thoracic Outlet Syndromes (TOSs): Neurogenic, Venous And Arterial
inconsistentnetherlandsneurogenicoutcomesoutletpatientsreportingseveritystandardizesurgerytalktextbookthoracic
Feasibility And Status Of A Combination Endovascular Aortic Valve Plus Stent Graft Conduit For Treatment Of Type A Aortic Dissections: What Patients Are Candidates
Feasibility And Status Of A Combination Endovascular Aortic Valve Plus Stent Graft Conduit For Treatment Of Type A Aortic Dissections: What Patients Are Candidates
acuteaortaaorticAortic Stent GraftascendingBCTbrachiocephaliccombiningdistaleligibleentireintimalmedialPathophysiologypatientsproximalqualifystentSTJSTJ / BCTterumotherapeuticthoracictreattubevalve
Venous Issues in Thoracic Outlet Syndrome: Lysis, Venoplasty, First Rib Resection: Staged Or Same Setting
Venous Issues in Thoracic Outlet Syndrome: Lysis, Venoplasty, First Rib Resection: Staged Or Same Setting
admissionanatomicangiojetangioplastyanticoagulationBoston ScientificbrachialCatheter-directed thrombectomycatheterscenterschroniccolorcompressiondecompressiondocumentedembolizationendoextrinsichospitalizationhypercoagulableinadequatelysismaximaloccludedoccludingocclusionoutletpatencyPatentpatientspercutaneousperipheral thrombectomy systemPTAresectionsinglestenosisstentingsubclaviansurgicallysymptomsyndromesystemictherapeuticthoracicthrombolysisthrombosistreatmentunderwentveinveinsvenogramvenographyvenousVenous angioplasty never with a stent
DEBATE: Not So: If Careful Technique Is Used, Completion Duplex Or Angiography Control Is Unnecessary And May Be Misleading
DEBATE: Not So: If Careful Technique Is Used, Completion Duplex Or Angiography Control Is Unnecessary And May Be Misleading
aschercarotidCarotid endarterectomyclampcompletioncomplicationdiagnosticexternalexternal carotidimaginglesionlesionsneurologicalpostoperativeratesresidualstenosisstrokesurgeonstechnicalunnecessary
Value Of A Vascular Surgeon To The Practice Of Other Specialties And To An Institution: How Can Vascular Surgeons Be Adequately Compensated By Institutions For Their Unique And Vital Contributions
Value Of A Vascular Surgeon To The Practice Of Other Specialties And To An Institution: How Can Vascular Surgeons Be Adequately Compensated By Institutions For Their Unique And Vital Contributions
aneurysmcardiaccenterscoworkersenablingendovascularfavorablehealthcarehospitalimpactmarginmedicareorthopedicpatientspayorprofessionalrevenuervusspecialtiesspinestentsurgeonsurgeonssurgeryvascularVeith
The Restenosis Rate After CAS Is Probably Higher Than After CEA In The RCTs: When Should Restenosis Be Treated Invasively
The Restenosis Rate After CAS Is Probably Higher Than After CEA In The RCTs: When Should Restenosis Be Treated Invasively
carotidclinicaldataduplexendarterectomyfreedomincidenceipsilateralkaplanlatemedicalmeierpeakprimaryproximalpublishedrandomizedrestenosisstenosissymptomsystolictherapytrialultrasoundvalidatedVeithvelocity
Near Infrared Spectrometry (NIRS) Monitoring Of Spinal Muscles To Reflect SCI With TAAA Repairs: How It Works And Early Experience
Near Infrared Spectrometry (NIRS) Monitoring Of Spinal Muscles To Reflect SCI With TAAA Repairs: How It Works And Early Experience
arteriesBEVARclinicalcollateralcorddopplerdorsalevarexperimentallaserlumbarmentoringmidlineMIS²ACEmonitoringnetworkneurologicocclusionoxygenationpatientreflectssegmentalsetupspectroscopyspinalspinestenttechnologytherapeuticvalidation
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
When Is Endovascular Treatment Of Erectile Dysfunction Indicated And Justified: Technique And Results
angioplastyanteriorarteriographyarteryballoonclinicalcontralateralcorrelatedDESdopplerdrugdrug elutingDrug eluting stentdysfunctionelutingendovascularerectileevaluationHigh grade bilateral internal pudendal artery stenosisiliacimprovementinternalInternal pudendal artery stentingMedtronicmultifactorialpatientsPOBAprocedurepudendalResolutestenosisstentstentedstentingStenting with a drug-eluting stentsystolictherapeutictreatment
DEBATE: EVAR Should Be The First Choice In Treating Mycotic AAAs: Based On A 10-Year Experience
DEBATE: EVAR Should Be The First Choice In Treating Mycotic AAAs: Based On A 10-Year Experience
aneurysmaneurysmsaorticCarotid-CarotidCarotid-LSA bypass TEVARChimney innominate a.complexendovascularerosionevarextendedfavorableFistulagraftinfectedInfected Arch Aneurysminfectionischemiamortalitymultiplemycoticpatientpatientsproximallysegmentstentsurvivaltherapeuticthoracictreatvenavertebralvisceral
Duplex Ultrasound As An Imaging Modality To Replace Angiography And Fluoroscopy In EVAR And Lower Extremity Interventions: Advantages And Limitations
Duplex Ultrasound As An Imaging Modality To Replace Angiography And Fluoroscopy In EVAR And Lower Extremity Interventions: Advantages And Limitations
angiographyarteryballoonbowelchronicclinicalcontrastcreatininedilatationduplexdynamicendovascularevarformationguidewirehabitusiliacinsufficiencypatientpatientspoplitealpublishedrecanalisationreductionrenalstenosisstenoticstentstentstasctreating
DEBATE: Not So: Advantages And Limitations Of The Supraclavicular And Infraclavicular Approaches For Venous TOS: Which Approach And When But Never Transaxillary
DEBATE: Not So: Advantages And Limitations Of The Supraclavicular And Infraclavicular Approaches For Venous TOS: Which Approach And When But Never Transaxillary
angiogramangioplastyanterioranticoagulationapproachaxillaryballoonBalloon angioplasty/stentsBothcollateralscryocyanosisdecompressionduplexexposurefavorablyFirst Rib ResectionfollowincisionsinnominateintraoperativeinvolveslymphaticneurogenicobstructionographypatientpatientsPlan for Surgical TreatmentposteriorpostoperativereconstructionresectedresectionScalenectomystenosisstentstentssubclavianSubclavian Vein ThrombosissuccessfulswellingthrombolysisThrombolysis / Balloon Angioplastyunderwentveinvenogramvenous
With Mural Thrombi In The Thoracic Aorta, When Do They Have To Be Treated Invasively: If They Do, TEVAR Is The Best Treatment: Precautions
With Mural Thrombi In The Thoracic Aorta, When Do They Have To Be Treated Invasively: If They Do, TEVAR Is The Best Treatment: Precautions
anticoagulationaortaaorticbarecontralateraldistalemboliembolismendovascularextremityfilteriliacsmuralpatientpatientsproximalrecurrentrepairstentstentssurgicalTEVARthoracicthrombithrombosisthrombustreatedtypevisceralwallstentwallstents
Treatment Strategies, Approaches, Technical Tips And Outcomes With Subclavian Artery Aneurysms
Treatment Strategies, Approaches, Technical Tips And Outcomes With Subclavian Artery Aneurysms
anatomicaneurysmsanomalousaorticarcharterialarterycervicalcommonlycompressionconcomitantconnectivedegenerativedistalendovascularextremitymortalityoriginatesoutcomesoutletpatientsposteriorproximalrepairsubclavianthoracic
Tips And Tricks In The Treatment Of Carotid Aneurysm: A Surgeon’s Perspective
Tips And Tricks In The Treatment Of Carotid Aneurysm: A Surgeon’s Perspective
accountinganeurysmaneurysmsanticoagulationapproacharteryatheroscleroticbasebifurcationcarotidcarotid arterycervicodiffersdiseasedysplasticendovascularetiologyhybridipsilateralligationmortalitymycoticneurologicocclusiveoccurringpatencyrarereconstructionreconstructiveReconstructive Aneurysmorrhaphyrevascularizationsaphenoussegmentsegmentssequelaeskullstentstentedstentingstentssurgerysurgicalsymptomstakayasutherapeuticthoracicthrombus
Transcript

couple of sample cases. I have pretty much a degenerative practice. I don't really do formal deformity very often but this is a bread-and-butter

type case. The patient previously had 5-1 fusion and stenosis and breakdown above. We used the my spine guides for both the thoracic and lumbar spine with exception of the levels immediately above the previous surgery as the guides were not

able to be used for those. Final results.

- [Karl Illig] Thanks Rob and Mark and thanks to Frank and the team for inviting me again. What they forgot to say is this is clearly the most exciting session of the whole VEITH meeting so you guys are lucky that you're here, you go got your seats early and we'll go from there.

So there's no conflict of interest to be had in TOS. My caveat is for the next four and a half minutes, I'm just really going to be talking about Neurogenic thoracic outlet system. So I was asked to talk about what's new and it's a little bit of a conundrum.

There's actually plenty new. I'm going to briefly review the reporting standards document that was published last year to sort of try to bring order to chaos. Also talk about a few selected publications over the last year or two.

Some international outreach efforts and there's another edition of the textbook coming out so love to chat with anybody who wants to be an author. So thoracic outlet syndrome and again, mostly neurogenic, suffers from inconsistent terminology, no agreement on diagnostic criteria and inconsistent

outcomes reporting. And as a result, we're not even sure what we're talking about. We're talking about the same thing. Very poor data. Sort of a negative feedback loop that we've got

no data, no good results, nobody likes it, it's very subjective, et cetera, et cetera. So a few years ago, it really spurred by the meeting that Rob held in St. Louis around 2009, 2010 or so, we came up with the society for vascular surgery reporting standards document.

Really three objectives. One is to standardize terminology. Number two is to standardize the diagnosis. And we don't pretend to have a cosmic knowledge of what it actually is. Depends on what the meaning of the word is is.

But we want everyone to be talking about the same thing and therefore standardize reporting requirements. At the bottom there, there's two references. One is the executive summary and one is the full document. Number one to diagnose TOS, neurogenic TOS, you need three of the following four criteria.

Pain, tenderness at the scalene triangle, tends to radiate around. It hurts when you press. There's a problem at the scalene triangle. Number two is distal neurological symptomatology. The nerves are being squeezed.

Tends to be worse with arms overhead, tends to be worse with dangling, et cetera et cetera. Number three is absence of other things that could cause these symptoms. And number four is positive response to a properly preformed scalene test injection.

Some people inject everybody, some people just use this as a tiebreaker in confusing situations. We ask people to ignore pulse obliteration. It's time that really went away. Many, many normal people obliterate and many people with neurogenic TOS do not.

It is not sensitive or specific enough. The physician ranks their severity as low, medium or high and the patient ranks the severity as low, medium or high. We ask for a QuickDASH and CBSQ on everybody.

Report outcomes primarily at three to twelve months but use life table analysis afterward and talk about it recurrence rate. How about some recent publications? There's a few interesting things out there. Bottros, a group from Washington University

described a stress block for those athletes who are only symptomatic during their athletic endeavors. I've contributed some patients to that and to my knowledge, our two groups together, we've never had anyone who has not recovered, who's had a positive block.

Dr. Peek from the Netherlands did a beautiful meta analysis and came up with numbers exactly what we quote from our experience. 90% of patients properly treated with surgery improve, and QuickDASH drops 28 points which is pretty nice. Rob Thompson next to me looked at his experience

with major league pitchers, found that about 80% return to full function and that's a pretty good number to tell your athletes. And Wooster from our group, we published a nice cocktail of pain medicine in addition to dropping the pain score, we reduced the our length of stay but a day and a half

which was kind of a nice thing. Now there's a talk I believe immediately following mine on robotic or thoracoscopic rib resection which I'm interested to hear. Couple of papers out, one from Lafosse in France. Again got a 90% improvement with the thoracoscopic

rib resection. I'm sorry, with just brachial plexus lysis, endoscopic lysis and professor George from England had 10 patients with thoracoscopic first rib resection. 9 of the 10 improved. So again, 90% success rate which I think

is a good number for the modern era. International outreach. I've heard TOS described as an American invention just to make money but I think more and more people now, especially in Europe and various places are getting interested.

I had conversation with two very interested people a couple of days ago which was a lot of fun. England's interested, France is interested, Netherlands has a great center. People from China are interested. And there's sort of a grassroots thing

sort of led by a non physician, kind of philanthropist millionaire called TOSCOE which is aiming to increase this in Europe. Finally, the textbook Thoracic Outlet Surgery came out in 2013. Interestingly we missed many topics

and many things have changed since then. So we're getting a lot of new chapters. So I would say, many of the editors are in this room and please talk to us. We're looking for interested people who are not only interested

but also can write specific things. So thank you very much, that's what new in TOS in five minutes.

- [Peter] Thanks Martin, Dr. Melina, thank you all for coming and for the invitation. I'm going to talk today about an experience that we've had in a multi-institutional standardized trial where everybody used exactly the same definitions and same data collection system in evaluating patients with aortic endograft infection.

This came out of a previous study that we had published in the Journal of Vascular Surgery of aortic graft infection, where only 5% were endografts. And since that time, as most of you know, endograft infection has become sort of the new epidemic. As many of you know, endografts do get infected

and there have been probably 35 papers related to specifically to endografts since 2005. And the incidence, although low, means that every one of us will encounter this if we do aortic surgery. This is the Low Frequency Disease Consortium

that we put together, and you can see multiple institutions, primarily from the United States participated and Matt Smeds was the first author on this using this system of standardized data collection. So it was a review of experiences at multiple institutions over 10 years,

looking at the end points of morbidity, mortality with operative repair and also with medical treatment of patients with aortic endograft. Now just this slide shows not to blame one graft or one, they are all vulnerable to endograft infection. And to my mind, no graft is protected from endograft

and there probably is not any superiority of one graft, whether in the abdominal or thoracic aorta position. If you look at patients as far as who were entered into this trial as far as morbidity and comorbidities as well as demographics, they have the usual distribution

with the exception of the issue, which I think is one of the primary messages, is it was surprising to us that 15% of people taken care of by our authors, they didn't necessarily do the first procedure, 15% had a known infection

at the time that the endograft was placed, and this seems to be an easily preventable risk factor. The imaging in the United States is primarily CT and white cell scanning. There are occasional patients with MR and with endoscopy.

If we look at the time to infection, these curves have been very consistent and are very similar to those for aortic graft infection with open repair. So open and endo and the types of organisms, as you can see, are mixed between primary gram positive,

gram negative, polymicrobial, and fungal. If we look at the complications that might have caused the graft infection, the endograft infection you can see here that there are several that are extremely important such as groin infection, a urinary tract infection,

or other simultaneous infection. And many of the patients had an endoleak which required repair. So the authors, when they were asked if they could identify the cause and the infection they identified below, the three below,

but particularly a contamination at the time of the initial procedure. If we look at the management what surprised us was although the traditional teaching is a patient should have an extra anatomic bypass. In fact, that only happened in 11 patients

and the majority of patients get either a cryopreserved allograft, a NAIS procedure, or a prosthetic is placed in situ, either soaked or nonsoaked. The complete excision was practiced by most of the authors here. This is a big operation.

And as you've heard before, pretty high risk, and often followed by wrapping of the graft after it's been placed, the new graft with omentum. Cryopreserved is also used, and this is just a diagram of how it might be placed and what position and the NAIS procedure,

which you've heard a nice description of before by Dr. Black. And the extra-anatomic bypass is the last option. If we look at the outcomes, blood loss was similar. Slightly larger with a NAIS which is a bigger procedure and realized that often that was two operating teams

that did that procedure. If we look at the complications, the 30-day mortality is 11% and the most important issue is one of persistent infection. If we look at the long-term survival, I've outlined in the red box the main issue, which is of graft displaced in situ,

a prosthetic graft, and not soaked in antibiotic. That seemed to be associated with a much higher mortality. And also we looked at medical management of patients. Now these are probably the highest risk patients. They were not candidates for open surgery, but they did quite poorly.

So in conclusion we believe that endograft infections are unique, that NAIS or cryopreserved antibiotic prosthetic grafts should be considered, and that the traditional approach of an extra-anatomic bypass is now not frequently used, at least in the United States.

Thanks very much for your attention.

- [Instructor] These are my disclosures concerning this presentation. Open thoracoabdominal repair still represents the state of the art for these complex diseases. However, even in most experienced centers complication rates following these procedures are serious, and despite high expertise this operation continues

to be very invasive for suffering patients of this disease. But also, the alternate techniques, like complete total endovascular repairs are associated with serious complications, a less 30 day mortality rate, but still high percentages of paraplegias and paraparesis,

a problem which is not solved, especially following these technologies. The idea for the SPIDER hybrid graft device came from the Frozen Elephant technique, which we use in a quite reversed technology. This enables us to perform this procedure

without total aortic crossclamping, we can avoid thoracotomy, avoid, also, extracorporeal circulation, and avoid spinal cord ischemia by reattachment of lumbar arteries. This is a video I would like to present you

following one of our pig models we operated on. You see here the SPIDER-graft with the stented proximal part completely in a sheath. Retroperitoneal approach to the abdominal aorta without dissection of the thorax and the diaphragm. And we start the procedure with attachment

of one of the branches to the distal part of the aorta by partial crossclamping of the distal aorta. This is the completed anastomosis. The second step now is introduction of the stented part of the graft. We did this here by a dissection of the celiac trunk

and introduced the graft via this hole into the descending part of this thoracic aorta, and we completely introduced this stent graft here. And then the sheath is removed, the splitter here, in a second step, also removed, and then the stent graft completely deployed.

This is the splitter which is removed here. And here now the stent is de-folded and completely expended. By doing so the entire blood flow now goes through the stent graft. And following de-airing through this side branch, which now performs, or enables, antegrade flow

to the legs, to the distal part of the body, and retrograde flow to all the visceral arteries. This is flow measurement, which we performed in all the side branches. And now we subsequently reattach all the visceral arteries via end to end anastomoses

starting with the celiac trunk, then followed by the superior mesenteric artery as you see here, and then I go over this both renal arteries, the right renal artery is reattached from inside the aorta.

And then, finally, the reattachment of the iliac arteries. This is final site following complete reconstruction. We performed in this series 18 domestic pigs with a variety of measurements here. And you see the results in terms of flow to all visceral arteries that

pre and post anastomosis flow was reestablished in a very nice way with very short clamping times. The perspective of this device is a variety of modifications. We introduced a nose cone for a guide wire, introducement technology,

reinforcement with double rings of the stent graft, then a side branch, and a SAFI loop for reattachment of the lumbar arteries. This is the team we performed these first animal studies with. And so I come to my conclusions

that hybrid graft implantation is technically feasible, crossclamping, visceral, renal, and spinal ischemia can be kept in very short limit. Thoracotomy, as well as extracorporeal circulation can be avoided. Modifications, however, are mandatory,

and the first in man study is planned. Thank you very much for your attention.

- Frank, thank you very much for your invitation. This is my disclosure. I think that all vascular surgeons are asking ourself following question. Is diameter of triple A the sole indicator for surgery? To ask for this question since about 20 years, we are interesting with function in aging with a PET CT

using 18F-FDG which allows the evaluation of the regional glucose metabolisms. And shows the presence of an inflammatory reaction at the level of atherosclerotic tissue infiltrated by the inflammatory cells. During our pilot study, we observed that

the uptake of the FDG was also stated with the unstable triple A. And during several studies, we were observed that FDG uptake not only show of predicted rupture but it predict also the site of the rupture

in triple A patients in Thoracic Aortic Aneurysms as well as Aortic Arch Aneurysm as you can see. Here is very easily we are find, you can observe FDG uptake and this patient we performed MRI and you can see here, free iron particles, it's same area of every velope. Starting increase FDG uptake

and this patient refused operation and come back three months later to rupture. Of course FDG is not specific for aneurysm or disease. We can found FDG uptake in cancer disease, infection or arthritis or arthritis and reason why several authors interested with different kind of biomarkers

and sodium fluoride F 18 each one of those one. And it's injections indicated for diagnostic PET imaging of bone to define areas of altered osteogenic activity. The primary clinical use of sodium fluoride PET is in detection of osseous prostate cancer metastasis. But some authors, all of them start to use it for

evaluation of the plaque metabolism in high cardiovascular risk subjects. One group from United Kingdom and leaded by a Dr. Newby from Cambridge, they performed several very nice studies using this marker in coronary artery disease for plaque rupture

and for evaluate aortic stenosis to accumulation of the calcification in the aortic leaflets. And also for carotid stenosis and they, during this several studies, they demonstrated that 18F sodium fluoride, selectively binds to microcalcification coronary

and carotid atherosclerotic plaques and that are associated with plaque vulnerability and rupture. More essentially he interested, they interest also the triple A and they called this study the SoFIA study and it concern about 72 cohort patients

and 20 study population. And it is very nice picture of the patients with positive 18F sodium fluoride uptake. It is specific for one and reason why it is left right in red color here, but anyways, very easy to show the infusion images uptake

at the symptomatic aneurysms. And they divided their cohort study in three levels of Tertile 1, Tertile 2, Tertile 3 according to sodium fluoride uptake from low uptake to increase uptake and they observed that the growth rate,

increased growth rate, aneurysm repair and rupture and aneurysm repair alone, it was significantly higher in the patients in Tertile 3 group. And they concluded that Fluorine-18 sodium PET-CT

is a novel and promising approach to the identification of disease activity in patients with triple A and is an additive predictor of aneurysm growth and future clinical events. My conclusion is 18F-FDG and 18F Sodium Fluoride however,

not specific for inflammation. Therefore, new imaging tracer for a more accurate inflammation detection and therapy evaluation are needed. We need specific markers of angiogenesis and inflammation to predict the triple A evolution and potential rupture.

Thank you very much for your attention.

- [Narrator] So this is actually a continuation of this discussion that we just heard about. Here are my disclosures. I don't think there's anything related to what I'm going to present. Now the endovascular repair of the ascending aortic aneurysm

has been achilles heel of this procedure for most of us for many, many years. And the reason for it is, a variety of scenarios that we have to deal with. One is anatomical complexities, such as the proximity of the coronary arteries, innominate and aortic valve.

Another one is inner curvature, and angulation of the inner curvature. There are hemodynamic forces that we have heard here, that affect the movement of the stent graft during the deployment. Respiratory motion as well,

and then several device issues because none of the devices that are commercially available at the present time are approved or designed for that particular indication. And they are large in profile, typically 22 and 24 French OD The issue frequently comes with a nose cone that is too long

and you almost invariably have to place it into the left ventricle to be able to complete the procedure. So the purpose of this presentation is to describe our technique of the least invasive approach for endovascular repair of Ascending Thoracic Aortic Aneurysm.

And here are two patients, so this is the first patient with a lot of co-morbid conditions as you can see. The diagnosis of the pseudoaneurysm was established after cardiac arrest. You can see he was truly a very sick man, with low ejection fraction and surgery was considered

to be a high risk procedure for him. So due to that we elected to perform this procedure, under local anesthesia, which we always do in a lot of scenarios, with EVAR, TEVAR and TAVR. Conscious sedation, percutaneous approach and using RV pacing.

Now RV pacing is very routine thing for us doing TAVR and it's really not an issue. It takes less than five minutes to put a pacemaker in the RV and we can test it for ten seconds to make sure we lower the blood pressure down to below 50 millimeters of mercury, which prevents

movement of the stent graft during the deployment. We us the standard technique that we use for TAVR, crossing the valve and placing stiff wire, typically Lunderquist wire in the LV, and then we use a device or stent graft, or our choice. In this particular scenario we used a Valiant,

this was under IDE and deployed a stent graft with rapid pacing as you can see here the blood pressure is below 50 millimeters of mercury, and that allows you accurate placement of the stent graft, in desired location and here you can see the final result, and no evidence of endoleak.

Pay attention that the distal part of the stent graft is open design, so that obviously allows flow to the coronary arteries and prevents really fixation of aortic valve leaflets. So this patient had uneventful post-operative course and was discharged the following day.

Now here is a second patient that had surgical repair of the ascending aortic aneurysm, and on the fifth post-operative day developed excruciating pain. Obtained an EKG, there were no abnormalities, the blood pressure was low,

we ordered a stat CT scan and he had this pseudoaneurysm which was between the graft that was placed there and a wrapped aorta around it and this was enlarging. So again, the patient refused another surgery, and we, again, performed this procedure percutaneously under local anesthesia.

Now this time we used a different graft. We used a Cook TBE 32 by 80 stent graft, and you can the Cook stent graft has a longer nose cone, so we had to place it all the way into the LV, over Lunderquist wire and even bend it around the stiff part of the Lunderquist wire,

which is a little bit scary in a lot of scenarios, but it worked well in this particular patient and we deployed the stent graft and there was no evidence of endoleak. The patient also did very well. This was conscious sedation and local anesthesia

and was discharged the following day. And here is his follow up at one month. And then we have also at six and one year follow up. No evidence of endoleak as you can see here. So, to the best of our knowledge, we are reporting the first experience of endovascular repair

of the Ascending Thoracic Aortic Aneurysm, with local anesthesia, conscious sedation, percutaneous approach and RV pacing. And I think this technique is indicated in very high risk patients that otherwise would have significant problems with surgery.

And obviously this offers a rapid recovery to most of the patients that undergo this procedure. But definitely there is a need for improvement in design and dedication of the stent grafts to this particular approach. Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Thank you for the invitation to discuss suprarenal bare stent fixation. Here are my disclosure. Aneurismal over graft extension is a part of the natural evolution and the natural history of this degenerative disease, and it could be extended to the celiac aorta

and the common iliac, as well. Regarding the extension to the celiac aorta, we have to consider the infrarenal aorta status, when we want to correct that, and mainly the lengths in between renal artery and the bifurcation of the previously implanted graft,

but also the quality of the access route from below. Most importantly is juxtarenal status, with or without bare stent, and we have nine cases of each. The way to correct this kind of failure is the use of chimney,

when fenistrated graft are not usable. And, the secondary chimney celiac extension, we have 18 cases, when there is a long aortic segment longer than 50 mm, we use a combination of a non-bare stent cuff, associated with balloon-expandable covered parallel stents.

And, when there is a short aortic segment, less than 50 mm, or a difficult access, we use an EVAS device, associated, the same way, with balloon-expandable parallel stents. When the juxtarenal aorta is free of bare stent, it's quite easy to place a wire and stents,

and there is no major contrast in between the different components of the chimney, whatever it is, a cuff extension or the use of an EVAS. It's quite different to when there is, when we have to perform a renal stenting over a bare stent, and you can see that we have to develop tricks

to stabilize a wire into the renal stent by aortic balloon, or by a renal balloon, or renal filter, but this kind of tricks are not working very well. And, we had, in some cases, the need for using push-up procedures, which means that we are exerting forces

onto the delivery system and there's a parallel stent, and that lead to compression in between the different components of this chimney. And, in addition, when there is a bare stent previously implanted, there are forces and there is room

for gutter and that's the way to get type 1 Endoleak. And, it's more difficult when the bare stent is creating a stenosis on the ostium of the renal artery, and we had here to place a stent, a bare stent, for angioplasties and to go to a push-up procedures, before implanting the endoaortic graft

and you can see that there is a lot of contrast, onto this renal stent. When there is a bare stent, there is a slight, the operating time is longer, and one type A Endoleak

more in the bare-stent population of patient but we have one occlusion stent on the non-bare stent group. Endoleak could be treated by embolization into the gutter. But, as we want to avoid this kind of difficult procedures, we use a classification,

based on the evolution profile of the aneurysm. When the neck are safe, we use EVAS to prevent type 2 Endoleak. When the neck is cylindrical, but slightly disease, we use a bifurcated graft, with infrarenal fixation. When the neck is short or when there is no neck,

we use four fenestrated graft, or tri-chimney procedures, and when there is a celiac aneurysm, we use thoracoabdominal reconstruction, using a thoracic segment, in addition with four-fenestrated graft, or a thoracic branch device.

Then, to conclude, the bare stent doesn't prevent the evolution of the aneurysmal disease, that means that we have to reconsider the use of endoaortic graft, with bare stent suprarenal fixation, just to anticipate what could happen during the evolution and the ability to perform

a secondary device extension. And thank you for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Jean] All right, thank you and good morning everybody. I'm going to go kind of quickly through this Early Feasibility Study that we initially started here in Houston across the three centers in Houston, so Methodist, Dr. Coselli's site, and Dr. Safi's site. Essentially it's the first industry sponsored,

FDA approved trial for endovascular repair of type A dissections. And really the goal here was to kind of understand what happens in these dissections when you treat them endovascularly. Also to guide future therapies in terms of design devices

for ascending dissections. The study population is limited to type I and type II dissections of DeBakey classification, and we're currently approved as far as the FDA for up to 10 patients. We have currently expanded to six US sites

as you can see listed there. Dr. Reardon is the principal investigator, National Principal Investigator, one of my cardiac partners at the hospital. As far as inclusion, exclusion criteria, the primary entry tear must be located in the ascending,

at least two centimeters distal to the most distal coronary artery ostia. It must be a high surgical risk and there are some criteria for that. Obviously most of these patients are high risk so that becomes a little bit of a judgment thing as well.

But we do have, we have developed some criteria for what we consider high risk. A lot of this was taken also from some of the high risk TAVR trials. We must have good quality imaging, and so what we've done is all patients get essentially

the same imaging that we have defined for TAVR, and so these are ECG gated CTs. Since they are re-imaged when they get to the hospital, these have to be fairly stable patients. The exclusion criteria, obviously moderate-to-severe aortic insufficiency,

valvular insufficiency, neurologic event at presentation, or known degenerative connective tissue disorders. The aortic extender has, to date, been the device we've used. There are a number of issues we've had with this device, and so I'll show you in next slides we have gone over

to a different device and have not started with that new device yet. The rest of the thoracic branch endovascular system is available in circumstances of complications. So we can use that as a bailout. We have not had to do that to date.

All implants to date, as mentioned there, have been isolated stent grafts to the ascending aorta, very much like you would do an open repair. The trial, as I mentioned, is currently expanded to six sites from three. The investigational device for all future implants

will be the Gore-- and a lot of the issues we've had. So some of the challenges are minimizing number of devices required. We've used up to four devices on some of these patients. Enhance conformability, optimize orthogonality

in the proximal ascending aorta, and then provide staged deployment. We've had four enrollments. They've all been at Methodist. Nobody else has enrolled any patients to date, and these have been as listed there.

Quality imaging and expertise is really critical. Again, a lot these lessons have been taken away from the TAVR population and some of the algorithms that seems has developed for TAVR cases. So fusion has been really at the top of our usage. Multifaceted imaging is needed.

So we need to know where the coronaries are, entry tear location, arch vessels, and so again multiple angles of the C-Arm are oftentimes used during these cases. It's impossible to visualize all important structures in one angiographic plane.

The expertise and rapid pacing is important. We've had one perforation from an anesthesiology placed lead. So that obviously can be an issue. And then crossing the aortic valve, there was a question to Dr. Dake earlier

about how to cross the valve. And really, I learned this from just scrubbing on valvuloplasties with a cardiologist and it's actually not as difficult as it seems. Although the tools that we use for crossing diseased valves and dissecting aortas is very different.

The lessons we've learned here are really what's going to carry it down the road. We're hoping to get the rest of our 10 cases here in the next year and hopefully give you some good results after that. Thank you.

- [Narrator] So this is actually a continuation of this discussion that we just heard about. Here are my disclosures. I don't think there's anything related to what I'm going to present. Now the endovascular repair of the ascending aortic aneurysm

has been achilles heel of this procedure for most of us for many, many years. And the reason for it is, a variety of scenarios that we have to deal with. One is anatomical complexities, such as the proximity of the coronary arteries, innominate and aortic valve.

Another one is inner curvature, and angulation of the inner curvature. There are hemodynamic forces that we have heard here, that affect the movement of the stent graft during the deployment. Respiratory motion as well,

and then several device issues because none of the devices that are commercially available at the present time are approved or designed for that particular indication. And they are large in profile, typically 22 and 24 French OD The issue frequently comes with a nose cone that is too long

and you almost invariably have to place it into the left ventricle to be able to complete the procedure. So the purpose of this presentation is to describe our technique of the least invasive approach for endovascular repair of Ascending Thoracic Aortic Aneurysm.

And here are two patients, so this is the first patient with a lot of co-morbid conditions as you can see. The diagnosis of the pseudoaneurysm was established after cardiac arrest. You can see he was truly a very sick man, with low ejection fraction and surgery was considered

to be a high risk procedure for him. So due to that we elected to perform this procedure, under local anesthesia, which we always do in a lot of scenarios, with EVAR, TEVAR and TAVR. Conscious sedation, percutaneous approach and using RV pacing.

Now RV pacing is very routine thing for us doing TAVR and it's really not an issue. It takes less than five minutes to put a pacemaker in the RV and we can test it for ten seconds to make sure we lower the blood pressure down to below 50 millimeters of mercury, which prevents

movement of the stent graft during the deployment. We us the standard technique that we use for TAVR, crossing the valve and placing stiff wire, typically Lunderquist wire in the LV, and then we use a device or stent graft, or our choice. In this particular scenario we used a Valiant,

this was under IDE and deployed a stent graft with rapid pacing as you can see here the blood pressure is below 50 millimeters of mercury, and that allows you accurate placement of the stent graft, in desired location and here you can see the final result, and no evidence of endoleak.

Pay attention that the distal part of the stent graft is open design, so that obviously allows flow to the coronary arteries and prevents really fixation of aortic valve leaflets. So this patient had uneventful post-operative course and was discharged the following day.

Now here is a second patient that had surgical repair of the ascending aortic aneurysm, and on the fifth post-operative day developed excruciating pain. Obtained an EKG, there were no abnormalities, the blood pressure was low,

we ordered a stat CT scan and he had this pseudoaneurysm which was between the graft that was placed there and a wrapped aorta around it and this was enlarging. So again, the patient refused another surgery, and we, again, performed this procedure percutaneously under local anesthesia.

Now this time we used a different graft. We used a Cook TBE 32 by 80 stent graft, and you can the Cook stent graft has a longer nose cone, so we had to place it all the way into the LV, over Lunderquist wire and even bend it around the stiff part of the Lunderquist wire,

which is a little bit scary in a lot of scenarios, but it worked well in this particular patient and we deployed the stent graft and there was no evidence of endoleak. The patient also did very well. This was conscious sedation and local anesthesia

and was discharged the following day. And here is his follow up at one month. And then we have also at six and one year follow up. No evidence of endoleak as you can see here. So, to the best of our knowledge, we are reporting the first experience of endovascular repair

of the Ascending Thoracic Aortic Aneurysm, with local anesthesia, conscious sedation, percutaneous approach and RV pacing. And I think this technique is indicated in very high risk patients that otherwise would have significant problems with surgery.

And obviously this offers a rapid recovery to most of the patients that undergo this procedure. But definitely there is a need for improvement in design and dedication of the stent grafts to this particular approach. Thank you very much for your attention.

- Thank you chairman, ladies and gentleman. Many thanks to the organizing committee for giving the opportunity to discuss this quite important issue. Well, if we look at the EVAR 1 and EVAR 2 trials you could see that there was a non-significant tendency towards cardiovascular deaths in the the endovascular group

during the 24-month interval. But cardiovascular morbidity and mortality was attributed to the required secondary interventions. Now the ACE study finish at the four-year followup 2007, and important survival free of reinterventions 78%. 10 years later the same people on the French Registry

reported a survival free of reinterventions 86% at four years, therefore an improvement. If we look at the mortality, four years mortality for the ACE study was 80%, and we look at the four years mortality for the registry is again 80%.

So cannot be only the rate of reinterventions. Now if we look at all the published results of the EVAR trials we can see that in the beginning there is a tendency in favor of failure regarding myocardial infarction, which is later on is lost and the diamond goes towards

the open repair. Arterial stiffness could be an explanation because arterial stiffening results in increased pulse pressure, left ventricular hypertrophy, subendocardial ischemia, endothelial dysfunction, and cardiac fibrosis.

And pulse wave velocity, it's a very easy way to measure arterial stiffness. You measure pulse wave velocity between the left carotid and the left common femoral, and we know from cardiologists' studies that pulse wave velocity is an independent predictor of cardiovascular morbidity and mortality.

There are other ways, like computational fluid dynamics, or elastography, or 4D MRI, but all these are cumbersome and quite expensive, so I believe pulse wave velocity is the best. So what is happening when you operate on a triple A? After an open repair you can see a modest increase

in pulse wave velocity while after EVAR you can see a statistically significant increase in pulse wave velocity at six months. And not only that, but novel biomarkers like OPG and interleukins are also increased, and these increases were pronounced in polyester woven group

compared to the PTFE group in this small study of 118 patients. Now what is happening with the heart? EVAR alters the cardiac structure and function as reported with this study from Japan, and induced left ventricular hypertrophy,

left atrium enlargement, and impaired diastolic function. And you can see here the exercise tolerance test that the compliance is worsening, pulse wave velocity's increasing, and the left atrial volume is also increasing. How about after thoracic endografting? Well, we did a little study on 27 patients

measuring pulse wave velocity and NT-proBNP changes in patients following TEVAR. I remind you that BNP's are coming from the cardiac myocytes as a sign of stress. So endovascular treatment of descending thoracic artery aneurysms was associated with significantly

increase in proBNP as you can see here, and arterial stiffness as well. So coming to my conclusions, I believe that TEVAR and EVAR are associated with lower perioperative mortality and morbidity rates compared to open surgical repair, but this advantage is blunted at long term,

mainly due to an increase in cardiovascular complications. But arterial stiffening, together with adverse cardiac function after stent graft implantation may explain this change in the long-term outcomes. There is some evidence of increased arterial stiffness after EVAR related to graft type,

and most importantly, I believe that arterial stiffness should be taken into consideration by the industry when designing new endografts. And in the meantime, the patients after endovascular treatment of aneurysms are in need of intensive cardiac followup and should be instructed accordingly.

I thank you very much for your attention. (applause)

- [Presenter] Thanks doctors, well I can shorten my title a little bit [Laughter] These are my disclosures. So before I get into the value of the vascular surgeon in the healthcare system I thought it's interesting to sort of look at

what vascular surgery may look like through an administrator's eyes, you know and in general in vascular surgery we have relatively poor payor mix, frequently more than 70% of our patients are Medicare beneficiaries, and the ones that are younger

than 65 cause of their lower socio-economic class are frequently on Medicaid. And also we do a lot of high-cost procedures, a good example of that is endovascular aneurysm repair. And you know, we looked at that a few years ago, and we compared the DRG reimbursements

to what it cost, and if you notice, you know, two-thirds of the DRG payment is consumed by the cost of the stent graft. Which really doesn't leave much left for other supplies and for salaries, and so in general we are running

about a $5000 negative margin per case. Despite this, there are three things where vascular surgeons do add value to the healthcare system. I think you can actually look at the P&L for vascular surgery and it's going to be positive. The vascular surgery is an enabling service,

every hospital wants a vascular surgeon because they want to be able to support their cardiologists, their spine surgeons, their oncologists, and urologists. And lastly I'll talk a few minutes about the benefit of a high vascular

case index on hospital revenue. So we looked at our own vascular surgery P&L over a six year period, and we were looking at physician-generated revenue as well as hospital-generated revenue through DRG and HBAS payments. The top line result is shown here,

and on the left in yellow are RVUs, its professional revenue indexed to inflation. And you can see that it's not a big surprise that physician revenue dropped around 21% over the six-year period. And the red is the hospital revenue.

But what's really interesting, what kind of demonstrates the value of vascular surgery, is if you look at the professional revenue per RVU, it's around $100. But then if you look at revenue that you bring in based on the hospital reimbursement,

based on your work, and index it to RVUs, it's around $500 per RVU. And you know in our own instance, at Dartmouth-Hitchcock, if you look at, take the technical and professional revenue, and you look at operating margin per case, you can see cardiac surgery which in most cases

is going to be, you know, doing pretty well $7500 a case, but you can see vascular surgery is relatively high up on the list there with a margin of around $2500 per procedure. Hospital medicine you might think is kind of an outlier, but at Dartmouth the orthopedic patients

are placed on the hospital medicine service. So when you look at vascular surgery as an enabling service line, Tonita and coworkers looked at 300 off-service patients over a four-year period, and you know in half the cases the

surgeons are doing spine exposure, in 14% they are doing vascular control prior to hemorrhage, and interestingly, in another 14% it was vascular control after hemorrhage. And then 19% of the patients required a vascular reconstruction,

and this generated around 1400 RVUs per year. And then lastly, just to say a couple words about Case Mix Index, this may be the most important and have the biggest impact on hospital reimbursement. Case Mix Index reflects the diversity and complexity of the patients a hospital cares for.

And the CMI affects hospital-wide Medicare reimbursement, so at our institution, each increase in the CMI of 0.01, which sounds like a small number, results in a $3 million increase in annual revenue. So here's a list of Case Mix Indexes from 2010 from various academic medical centers in the United States.

And you can see at Dartmouth-Hitchcock, so our hospital is around 2.13, the section of vascular surgeries' CMIs increased during this time from 2.4 up to 2.8. And so obviously we're going to have a positive impact on the hospital's CMI.

And then the question is, well where might we fit in sort of with the specialties that are typically associated with the heart and vascular center. And you can see the CMI for cardiac surgery, and this is pretty typical throughout,

from institution to institution, is around five and a half, and vascular surgery is at 2.8, and cardiology is around 1.87. And the hospital CMI is 2.13. So we're, we are contributing to increasing the CMI, which is going to have a significant

impact on hospital revenue. So in conclusion, vascular surgery technical revenue really drives the majority of hospital vascular reimbursement. And the vascular surgery presence allows for safe conduct of many additional highly reimbursed procedures.

Favorable vascular surgery CMI improves hospital-wide reimbursement from CMS, and while RVUs can measure productivity, they are not a good measure of value of the vascular surgeon. Thank you, I'd like to thank Dr. Veith for

the privilege of inviting me to this outstanding meeting. Thanks.

- [Presenter] Thanks, Frank, for another phenomenal meeting, but special thanks for forcing us to condense our thoughts into five minutes. It's a really wonderful exercise. I personally appreciate it very much. We're going to spend the next few minutes talking about what I think is the next horizon,

which is basically looking at cognition as an outcome. I'll say it later, but cognition, we don't really have a handle on this at all. Conflicts. I will mention Silk Road, and I do have a conflict there. Get the artery open is what this is all about.

As fast as possible. Less than two hours, if at all possible, because the new data really, really nails that as the time that we have to shoot for. As we all probably know, well, most of the cerebral damage that we get

from all interventional procedures is subclinical, we just don't see it, we don't have the tools to evaluate it, but it is a major, major problem for us, I think particularly when you look down the road. What's the impact on these patients?

Is it much like is happening in the National Football League, where these minor traumas end up causing dementia? I think it is, and we have to really be aware of that. What have we learned about neurologic injury post intervention?

First, the clinical need for neuro protection is quite obvious with a lot of these procedures. Second, intervention procedures proximal to the brain definitely release debris. We've seen that over and over again. Imaging studies consistently show

DWI evidence of that debris being released. The pharmacological approaches don't work. There's mounting evidence that shows that new infarcts, I mean DWI lesions without clinical evidence, cause neurocognitive defects and/or predispose our patients to later problems, degenerative disease.

Embolic protection. The difference between carotid stenting and other vascular procedures is really interesting. The need for embolic protection with stenting of the carotid was obvious. The trials mandated embolic protection in spite

of the fact that we had no evidence at all, no randomized data, that proved that protection worked. DWI lesions are much greater post carotid stenting than they are post carotid endarterectomy. We're not 100% sure what that means, but it's getting more and more clear

that it does mean something significant. Looking at some of the other interventional procedures that we all see, TAVR, SAVR, left heart and aortic interventions, there is no mandate, because it wasn't obvious in the beginning that treating these lesions

was going to release so much debris into the brain. The real wake up call was the studies that showed a stroke incidence, anywhere from 2% or 3% all the way up to 17% in one major study. A look at the TAVR and left heart story is really interesting.

First of all, if you look at the MRI composite data from some of the TAVR studies, this one happens to be from the CLEAN-TAVI study, showing all this DWI change in the brain. This cannot be good. Why do these lesions matter?

We have mounting evidence with lots of studies now coming on board showing us scientific evidence that these DWI lesions do lead to problems later on. What about carotid stenting? Just to mention it, it is certainly growing in popularity, but it's not there yet.

CEA is a safe, effective, and stable procedure, and for stenting to be a major player, it has to be equal to carotid stenting. When we look at carotid stenting early studies, DWI hits 40% to 70%. That's not acceptable.

Bill just showed you a nice reduction in that with one technology, but we've seen amazing technology evolution in carotid stenting in spite of the problems that we see, and that technology's evolved from balloons to filters and so on,

to the direct carotid approach with Silk Road, which has seen a major reimbursement shift, and mesh covered stents that also, I think, are going to play a major role. Early trials in TAVR, a stroke rate 2% to 4%. No question there was something not quite right there.

The big thing was, in the filter study, 98% of the filters had recognizable debris. It's obvious why. Look at the aortic arch and the valve that we're treating. Everything from valves to even pieces of the device have been collected in these filters.

Just look at this and it makes you sick. The neurocognitive studies, they're all over the map. They don't give us any definite answer, and we need a lot more work on neurocognitive studies. Our conclusion is that all these procedures release debris, all result in DWI lesions.

This cannot be a good thing. We need standardized, reliable, easy and repeatable testing of cognitive function, and we obviously need safe embolic protection. Thank you.

- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.

And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.

Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.

Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.

It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,

if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?

You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you

about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,

and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may

be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.

A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased

the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,

and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.

But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history

or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?

Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because

more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.

Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.

They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.

To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history

in various degrees of relatives. So with that, thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Karl Illig] Thanks Rob and Mark and thanks to Frank and the team for inviting me again. What they forgot to say is this is clearly the most exciting session of the whole VEITH meeting so you guys are lucky that you're here, you go got your seats early and we'll go from there.

So there's no conflict of interest to be had in TOS. My caveat is for the next four and a half minutes, I'm just really going to be talking about Neurogenic thoracic outlet system. So I was asked to talk about what's new and it's a little bit of a conundrum.

There's actually plenty new. I'm going to briefly review the reporting standards document that was published last year to sort of try to bring order to chaos. Also talk about a few selected publications over the last year or two.

Some international outreach efforts and there's another edition of the textbook coming out so love to chat with anybody who wants to be an author. So thoracic outlet syndrome and again, mostly neurogenic, suffers from inconsistent terminology, no agreement on diagnostic criteria and inconsistent

outcomes reporting. And as a result, we're not even sure what we're talking about. We're talking about the same thing. Very poor data. Sort of a negative feedback loop that we've got

no data, no good results, nobody likes it, it's very subjective, et cetera, et cetera. So a few years ago, it really spurred by the meeting that Rob held in St. Louis around 2009, 2010 or so, we came up with the society for vascular surgery reporting standards document.

Really three objectives. One is to standardize terminology. Number two is to standardize the diagnosis. And we don't pretend to have a cosmic knowledge of what it actually is. Depends on what the meaning of the word is is.

But we want everyone to be talking about the same thing and therefore standardize reporting requirements. At the bottom there, there's two references. One is the executive summary and one is the full document. Number one to diagnose TOS, neurogenic TOS, you need three of the following four criteria.

Pain, tenderness at the scalene triangle, tends to radiate around. It hurts when you press. There's a problem at the scalene triangle. Number two is distal neurological symptomatology. The nerves are being squeezed.

Tends to be worse with arms overhead, tends to be worse with dangling, et cetera et cetera. Number three is absence of other things that could cause these symptoms. And number four is positive response to a properly preformed scalene test injection.

Some people inject everybody, some people just use this as a tiebreaker in confusing situations. We ask people to ignore pulse obliteration. It's time that really went away. Many, many normal people obliterate and many people with neurogenic TOS do not.

It is not sensitive or specific enough. The physician ranks their severity as low, medium or high and the patient ranks the severity as low, medium or high. We ask for a QuickDASH and CBSQ on everybody.

Report outcomes primarily at three to twelve months but use life table analysis afterward and talk about it recurrence rate. How about some recent publications? There's a few interesting things out there. Bottros, a group from Washington University

described a stress block for those athletes who are only symptomatic during their athletic endeavors. I've contributed some patients to that and to my knowledge, our two groups together, we've never had anyone who has not recovered, who's had a positive block.

Dr. Peek from the Netherlands did a beautiful meta analysis and came up with numbers exactly what we quote from our experience. 90% of patients properly treated with surgery improve, and QuickDASH drops 28 points which is pretty nice. Rob Thompson next to me looked at his experience

with major league pitchers, found that about 80% return to full function and that's a pretty good number to tell your athletes. And Wooster from our group, we published a nice cocktail of pain medicine in addition to dropping the pain score, we reduced the our length of stay but a day and a half

which was kind of a nice thing. Now there's a talk I believe immediately following mine on robotic or thoracoscopic rib resection which I'm interested to hear. Couple of papers out, one from Lafosse in France. Again got a 90% improvement with the thoracoscopic

rib resection. I'm sorry, with just brachial plexus lysis, endoscopic lysis and professor George from England had 10 patients with thoracoscopic first rib resection. 9 of the 10 improved. So again, 90% success rate which I think

is a good number for the modern era. International outreach. I've heard TOS described as an American invention just to make money but I think more and more people now, especially in Europe and various places are getting interested.

I had conversation with two very interested people a couple of days ago which was a lot of fun. England's interested, France is interested, Netherlands has a great center. People from China are interested. And there's sort of a grassroots thing

sort of led by a non physician, kind of philanthropist millionaire called TOSCOE which is aiming to increase this in Europe. Finally, the textbook Thoracic Outlet Surgery came out in 2013. Interestingly we missed many topics

and many things have changed since then. So we're getting a lot of new chapters. So I would say, many of the editors are in this room and please talk to us. We're looking for interested people who are not only interested

but also can write specific things. So thank you very much, that's what new in TOS in five minutes.

- (inaudible) Actually, just a short glimpse of what we're doing and of these, 2/3 of patients would actually qualify for some kind of a valve conduit. Well, actually, the proximal thoracic aorta is different. And this fundamental difference is pretty much related to the amount of elastic fibers.

The more proximal, the more elastic, and the more a compliance mismatch between a stent-graft and the native tissue, when it comes to endotherapy. And actually, anybody who has ever seen this kind of interpretive picture from the acute (inaudible)

will be clear that the tube alone will never be sufficient to treat the entire thoracic aortic disease. So actually, here this slide nicely shows all the challenges we are confronted with when going to an end approach.

The primary entrance is always near to the sinotubular junction. There's always a retrograde component, and the only component of the aortic route being not affected by the underlying disease is the aortic analys.

And this is a TEE of an acute aortic dissection, showing you the dynamics of the disease, and how stiff the entire segment becomes after TEVAR. So in order to address the pathology appropriately, we do have to understand what dissection, or how geometry changes occur by the dissection.

And actually, the main message here is that the ring acute aortic dissection ascending diameter increases by 30% in the mid-ascending aorta. So in other words, we have to rethink the entire issue, because the strategy has to be under-sizing and not over-sizing, to have the (inaudible)

back to the intimal medial cylinder. This is actually how we started. These were our first attempts in bench and bedside, and actually one issue we already overcame was the issue of perpendicular alignment of the graft to the sinotubular junction.

But still, just very few patients were eligible due to the lack of a valve. So again, to show you the main issue is that the primary entrance is always near to the sinotubular junction, and you will never have a landing zone,

you will just have a sealing zone. So this is how the first prototype we constructed looked like. And actually, this is our current experimental setup combining a Simitis Valve with a Terumo Aortic stent graft. And here you can see an animal implant

via a transapical approach, like we would do in routine TAVI. And actually, in the acute setting, this works very well. So patient eligibility. So radial force is distributed to the sinotubular junction, and at the level of the brachiocephalic trunk.

And actually, what we did, we went through a few hundreds of CT scans, and did a morphometry how the devices should look like, and who will finally by eligible. And actually, this is one of the main message. Up to 70% of patients are eligible for an endoconduit, if you have this kind of approach.

These are the measurements: root measurements, ascending measurements, distances. And finally, that's the bottom line. Eight stent-graft lengths would be required to treat all these patients being eligible. And finally, 1/3 of patients would qualify

for straight graft, and the remaining ones for tapered grafts in various extent. So, substantial differences in diameters of the proximal and distal ascending aorta requires tapering in several subjects. So summarizing, a thorough understanding

and a rethinking of the pathophysiology is key to success, complexity is amplified as compared to distal aortic segments, and the tube alone is never sufficient to treat the majority of patients, endoconduit is already a clinical reality,

and combining knowledge and technology will further pave the way. Thank you.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Presenter] Thanks doctors, well I can shorten my title a little bit [Laughter] These are my disclosures. So before I get into the value of the vascular surgeon in the healthcare system I thought it's interesting to sort of look at

what vascular surgery may look like through an administrator's eyes, you know and in general in vascular surgery we have relatively poor payor mix, frequently more than 70% of our patients are Medicare beneficiaries, and the ones that are younger

than 65 cause of their lower socio-economic class are frequently on Medicaid. And also we do a lot of high-cost procedures, a good example of that is endovascular aneurysm repair. And you know, we looked at that a few years ago, and we compared the DRG reimbursements

to what it cost, and if you notice, you know, two-thirds of the DRG payment is consumed by the cost of the stent graft. Which really doesn't leave much left for other supplies and for salaries, and so in general we are running

about a $5000 negative margin per case. Despite this, there are three things where vascular surgeons do add value to the healthcare system. I think you can actually look at the P&L for vascular surgery and it's going to be positive. The vascular surgery is an enabling service,

every hospital wants a vascular surgeon because they want to be able to support their cardiologists, their spine surgeons, their oncologists, and urologists. And lastly I'll talk a few minutes about the benefit of a high vascular

case index on hospital revenue. So we looked at our own vascular surgery P&L over a six year period, and we were looking at physician-generated revenue as well as hospital-generated revenue through DRG and HBAS payments. The top line result is shown here,

and on the left in yellow are RVUs, its professional revenue indexed to inflation. And you can see that it's not a big surprise that physician revenue dropped around 21% over the six-year period. And the red is the hospital revenue.

But what's really interesting, what kind of demonstrates the value of vascular surgery, is if you look at the professional revenue per RVU, it's around $100. But then if you look at revenue that you bring in based on the hospital reimbursement,

based on your work, and index it to RVUs, it's around $500 per RVU. And you know in our own instance, at Dartmouth-Hitchcock, if you look at, take the technical and professional revenue, and you look at operating margin per case, you can see cardiac surgery which in most cases

is going to be, you know, doing pretty well $7500 a case, but you can see vascular surgery is relatively high up on the list there with a margin of around $2500 per procedure. Hospital medicine you might think is kind of an outlier, but at Dartmouth the orthopedic patients

are placed on the hospital medicine service. So when you look at vascular surgery as an enabling service line, Tonita and coworkers looked at 300 off-service patients over a four-year period, and you know in half the cases the

surgeons are doing spine exposure, in 14% they are doing vascular control prior to hemorrhage, and interestingly, in another 14% it was vascular control after hemorrhage. And then 19% of the patients required a vascular reconstruction,

and this generated around 1400 RVUs per year. And then lastly, just to say a couple words about Case Mix Index, this may be the most important and have the biggest impact on hospital reimbursement. Case Mix Index reflects the diversity and complexity of the patients a hospital cares for.

And the CMI affects hospital-wide Medicare reimbursement, so at our institution, each increase in the CMI of 0.01, which sounds like a small number, results in a $3 million increase in annual revenue. So here's a list of Case Mix Indexes from 2010 from various academic medical centers in the United States.

And you can see at Dartmouth-Hitchcock, so our hospital is around 2.13, the section of vascular surgeries' CMIs increased during this time from 2.4 up to 2.8. And so obviously we're going to have a positive impact on the hospital's CMI.

And then the question is, well where might we fit in sort of with the specialties that are typically associated with the heart and vascular center. And you can see the CMI for cardiac surgery, and this is pretty typical throughout,

from institution to institution, is around five and a half, and vascular surgery is at 2.8, and cardiology is around 1.87. And the hospital CMI is 2.13. So we're, we are contributing to increasing the CMI, which is going to have a significant

impact on hospital revenue. So in conclusion, vascular surgery technical revenue really drives the majority of hospital vascular reimbursement. And the vascular surgery presence allows for safe conduct of many additional highly reimbursed procedures.

Favorable vascular surgery CMI improves hospital-wide reimbursement from CMS, and while RVUs can measure productivity, they are not a good measure of value of the vascular surgeon. Thank you, I'd like to thank Dr. Veith for

the privilege of inviting me to this outstanding meeting. Thanks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- Now we are delighted that there's apparently two things that we came up with years ago proved useful. This is the Near-Infrared Spectroscopy slide by Joe Bavaria from UPENN providing patient data on delayed paraplegia. That's a problem that we see in open NN (mumbles) very frequently.

How does the NIRS work? And again to this illustrative picture and now imagine the spinal cord sitting here in the spine canal and there's no more blood flow and this is the end result. When you know the oxygenation in the collateral network

and there was the problem with this technology that had been attempted 12 years back already, in Houston, I bet they put the NIRS optodes in the midline and the light cannot penetrate bone so it didn't work. But if you put it on the collateral network

and you measure the oxygen in this area, you obviously know it in the spinal canal. Dorsal view, again, so this is position of the optodes and this is oxygen content way interested in it. This is another cast just to illustrate

how these segmentals are regionally connected into the spinal canal, obviously. Experimental validation and pilot series in the next two minutes. Experimental cross clamping, this is the setup so years mentoring Laser Doppler Flow

to a real time evaluation of what you measure with your infrared setup in the animal lab and we see here, correlation is very nice between the lumbar NIRS, optodes, and the actual lumbar spinal cord oxygenation measured by Laser Doppler which is evaluated

with other techniques. Very nice to see the corelation between the two. So lumbar collateral network NIRS directly reflects spinal cord tissue oxygenation. After we have proven that step, next step was serial segmental artery occlusion.

As this is a technology that we or the strategy that we using, obviously want to know with our monitoring works for that. You see here, experimental setup basically the same. Starts with anesthesia, exposure of the segmentals. Now an open approach

and then you get 120 minutes surveillance period. You got a drop or dip in the NIRS measurements. Interestingly in the experimental setup in the recovery group, you see here that the new logical function comes back after the procedure and the NIRS comes back after the procedure.

Paraplegic group, all segmentals sacrificed NIRS, drops after the procedure in the first couple days, and the neurologic function does not recover. So experimental evidence that actually works. Nice corelation, again, so the experimental validation proves that lumbar NIRS

reflects lumbar spinal cord oxygenation and reacts to occlusion, of segmental arteries in real-time, but careful it's only regional so where ever you put your optodes, this is the area where you can monitor

your collateral network associated dip when you coil or include the segmental arteries. First clinical results published a couple years ago, I think you have all seen this video. Optodes are putting in the back of the patient, same setup for endo and open

and then we take the monitors theory and we have real-time monitoring on oversights midline here, this is (mumbles). Concept validation from 2016 with the first clinical data and now we're working on the clinical evaluation

of the use of this technology in EVAR and in clinical coil-embolization. 11 patients have been included so far for the EVAR group and you see here, it is very sensitive when you put stent in, stent deployment, but we have to still work so to speak

on the area that we have to monitor. There's a lot of work to do and probably also device modifications are necessary. MISACE, last couple words, on this you see pretty stable, NIRS all over the time course and actually this is nothing we wouldn't have expected

because the patient obviously were protected from spine cord anesthesia. So also here but sometimes we see a significant drop and this is when you should be careful and that's when you usually stop the procedure. So in conclusion, minor changes

in Collateral Network oxygenation have been seen in EVAR in this preliminary results using the nearest technology and to establish one very nice ... Nicely how clinical practice is already guided at his institution.

There's no immediate complete occlusion of covered segmental arteries and there's ongoing study in very heterogeneous patient group. There's no relevant changes with the chlorine technology so far,

but that, just to remind you, is the purpose of this technology, that we do not harm the patient during the preparation period. Thank you very much for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

- [Dr. Boonprasit Kritpracha] Thank you Mr. Chairman Good morning everyone. I'm here this morning to share with you our belief based on our and other experiences that EVAR should be the first choice to treat patients with mycotic aortic aneurysms. A disclosure.

We are dealing with two issues here. Aortic infection and the weakened of the aortic wall. Most common mortality in these groups of patients are from ruptured aneurysm and, second, by sepsis. That's why medical treatment alone is never a good option. What about open surgery?

The results are all over the board. The literature, we can see the mortality of even 0% like in this example of the cases. But when we look at the cases, these are early aortitis, some not even an aneurysm yet. We are talking about the infected aneurysm like this,

extension like this, complication like this, or at the difficult segment, multiple segments, or even at the aortic arch. And we are saying that open repair will offer a good reasonable result worldwide. Mortality rate reports in this kind of cohort

is over 30% in the literature. What about endovascular therapy? Of course, there is zero percent mortality reported, but we are looking at the more, bigger population more real world population, we can see the mortality from this study is 9%.

You see this before, interesting trend in Sweden. And you can see that EVAR provide a better short and medium term survival and comparable long-term survival compared to open surgery. Significantly, infection related mortality in both EVAR and open surgery,

long-term infection related mortality was comparable. But, look at our 12 year experience of treating infected aortic aneurysms patients using endovascular therapy. We had 26 at a thoracic level, 84 in the abdominal, three patients with both segments involved

and ten patients had infection at the major visceral vessel area. Altogether, there was 123 cases. We divided patients into fistula and non-fistula groups and we believe they are different. When we look at the non-fistula group,

the majority of the cases are presented quite late in our patients. These are extensive inflammation, leakage, huge leakage, and sometimes they come with a complication, because of the aneurysm compressed caused deep vein thrombosis that extended

into the inferior vena cava, or erosion of the vertebral body. These are the big three in our cause of problems in our area. Our in-hospital mortality was 9.8%, only 5.7% in the non-fistula group,

with all those complex anatomy. 32% in the fistula group. We followed these patients carefully, clinically and imaging studies. You can see some of the examples I was showing you, these patients we followed up for ten years, good results.

This huge leakage patient we followed this patient up to eight years, also good result. HIV positive, we have a few of these, and this patient up to five years, also good results. Vertebral body erosion slowly comes back, even with multiple segment involvement like this,

we did some monitoring of his treatment, so far so good, we haven't had any problem with spinal cord ischemia just yet in these three cases, but good results anyhow. In difficult anatomy like this, we use chimney procedure poly-graph I will say, we try to avoid three or four graphs at the same level.

In this case, we used two chimneys and two sandwich, good results. Another segment disease we bring two up and two down, good results, this case up to three and a half years. Even at the aortic arch level, this very sick patient came and the infection extended down to the mediastinum.

We used a minimal invasive way to treat this very sick patient, good result up to two and a half years. So far we've got favorable mid and long term results, we haven't seen any stent graft infection yet. Of course, there are some problems.

This patient, came with the aorto-caval fistula, did not respond well, so we have to open and remove the stent graft. Quite straight-forward procedure, considering that this patient came with a aorto-caval fistula in the first place.

We have to make sure that our stent graft extended beyond the diseased segment. Both proximally and distally. Endovascular therapy, even with this complex disease can provide quite a low mortality, less than 10%. That's why we believe that endovascular therapy

should be the first choice to treat patients with mycotic aortic aneurysms. We can leave it as a definitive treatment, or maybe as a bridging procedure. So Mr. Chairman, ladies and gentlemen, EVAR plus long-term antibiotics are effective

in both simple and complex anatomy, and it should be the first choice to treat patients with mycotic aortic aneurysm. Thank you for your attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

paraclavicular decompression. Thank you for your attention.

- [Ramesh] I'm going to talk about mural thrombi in the thoracic aorta when do they have to be treated invasively and is TEVAR the best treatment? As you all know that anticoagulation has been the main treatment of thoracic thrombus for a long time, in my opinion it's basically a nihilistic treatment

of primary or secondary aortic mural thrombosis mainly because the persistence of thrombus load or recurrent embolism risk is high with anticoagulation more than a quarter of the patients do have that despite anticoagulation and the same is true with surgical removal

at a level of 9%. The recurrent embolism significantly increases the risk of major amputation, it's 9% for anticoagulation alone verses 2.3% for the surgical group and life threatening visceral ischemia.

A recent meta-analysis did show that majority of the patients present symptomatically with lower extremity or visceral emboli so it's quite a deadly disease. Very few patients are discovered incidentally. We published a report on primary aortic mural thrombosis

and we divided the aorta into various segments and today we are going to talk about type two lesions, they are divided by the T eight spine into two a, which is proximal to T eight, and two b, which is distal T eight. The analysis of

of the descending thoracic aortic mural thrombus reveals that majority of the patients are now being treated with TEVAR in comparison to open surgery or anticoagulation. And if you look at the death rates and persistent thrombus rates, they are the lowest

with TEVARs compared to open repair or with anticoagulation. Our findings were similar and we found that whenever feasible endovascular repair should be done what we advocated is TEVAR for type two a lesions and bare-metal stents like the large-diameter Wallstents

for type two b lesions, especially in the wake of chances of spinal ischemia. This is one such case of type two PAMT and as you can see this was treated by TEVAR successfully. And this is a type two b PAMT and closed with bare metal stent.

And out of the eight patients we had excellent results in six patients and they were discharged, one patient underwent embolism, visceral embolism, and died because we couldn't get the covered stent in time. And the last patient had minor complications. We advocated that one of the precautions to take

during the endovascular coverage of this thrombus is a, to avoid major manipulation around the thrombus, as well as a endovascular filter which can be introduced from the contralateral groin. And this was a Wallstent that my colleagues were able to use in a emergency setting

and this is what we advocate now and this filter is effective and is able to capture major thrombi and bring it into iliacs from there it can be embolectomized. So ladies and gentlemen, the management of symptomatic PAMT type two is essentially in the asymptomatic patient

if the thrombus is sessile, we continue to do anticoagulation, if it's a mobile or floating thrombus or occupying more than 3/4 of the diameter, or is symptomatic, then these patients undergo anticoagulation,

TEVAR if it's type two a, bare stent or TEVAR if it's type two b. If it's type one then we also do arch debranching and of course we use distal protection as much as possible. Thank you for your kind attention.

- [Robyn] Thank you for asking me to speak. I have no disclosures. Subclavian artery aneurysms are quite rare, making up only 5% of all aneurysms. However, they do make up 50% of all supra-aortic aneurysms. They come in two locations, first, proximal, located in the chest, these are usually

degenerative in nature and they have other conditions, such as connective tissue disorders, fibromuscular dysplasia, and vasculitis associated with them. They also commonly have concomitant thoracic aortic aneurysms. The second type that we've been discussing this last talk

are distal aneurysms, which are usually related to arterial thoracic outlet. Patients may present asymptomatic. Symptoms include pain, which usually is consistent with rupture, upper extremity ischemia, including claudication, rest pain, Raynaud's, or

thromboemboli, or possibly, posterior circulation stroke. A physical examination should be focused on evidence of distal ischemia or concomitant aneurysms, and diagnostic evaluation is usually good with a CTA for both diagnosis, as well as surgical planning, and as

we discussed in the last talk, digital subtraction imaging is needed if there's evidence of distal ischemia. Traditionally, degenerative aneurysms were treated with open surgery, the right subclavian can be approached through a median sternotomy, with possible extension into a collar incision.

The left subclavian is approached through a left anterior thoracotomy. Once inside the chest, there's multiple ways to repair the subclavian artery. If only a subclavian artery is involved, a primary aneurysmorphy may be done

versus over-sewing the aortic stump and an extra anatomic bypass, however, often, the aorta is also involved, and this may require cardiopulmonary bypass, replacement of the aortic section, and possible debranching, or extra anatomic bypass.

From the area of endovascular surgery, we can now often repair these without having to enter the chest. This can be done with primary stenting if it's just a subclavian artery, however, proximal and distal landing zone

is required proximal to the take off of the vertival artery. If there's no proximal landing zone, or the aortic arch is also involved, a TEVAR can be done with either extra anatomic bypass, a subclavian snorkel, or now, using new branched endo devices.

Due to the rarity of disease, there's not much in the literature pertaining to outcomes of these aneurysms. This study from the time of open surgery looked at 27 patients that had innominate artery aneurysm repairs, and as I discussed, many of them have concomitant diseases, and vasculitis.

About half of them required aortic artery placement, as well, and outcomes were mainly based on how the patients presented. Those that presented with a rupture had an up to 50% mortality rate, while those that presented electively had only a 5% mortality rate.

From the era of endovascular surgery, the dupe group looked at 24 patients and had similar results, with 21% of the patients having a connective tissue disorder, and about half of the patients having concomitant aortic disease.

They were able to repair 64% with endovascular techniques, and had a similar mortality rate to that seen with open surgery of 5% for elective cases. Moving on to distal subclavian aneurysms, as our last speaker discussed, they are related to thoracic outlets, and therefore,

when repairing them, attention need to be paid to first relieving the arterial compression, then removing the source of embolism, and finally, restoring distal circulation. The best approach to relieve that compression is through supraclavicular incision.

This facilitates removal of the cervical rib and gives the best arterial exposure. An infraclavicular incision may also be needed to facilitate the distal anastomosis. Particularly about cervical ribs, in the population cervical ribs are quite rare,

occurring in only about 1% of the population. However, they are seen up to about 75% of the time in arterial thoracic outlet syndrome. The cervical rib originates from C7, and commonly has fibrous bands to the first rib that lie within the middle scalene,

which cases the compression on the subclavian artery. Therefore, both the cervical rib and the first rib need to be excised together. This is in comparison to an anomalous first rib. That originates from T1, and usually can be removed on its own.

Moving on to arterial interventions as our last speaker stated, again, once the rib is removed the artery is well exposed and a traditional aneurysmorphy can usually be done to fix the subclavian artery, taking care to deal with any distal embolization

with embolectomy at the time. Looking at outcomes, our moderator, Doctor Thompson, looked at 40 patients that they did at their group, and showed that it was about 50% of the patients presented with upper extremity ischemia,

5% presented with a posterior stroke, 75% had a cervical rib, and 12% had an anomalous first rib. They had to manage 70% of patients with their subclavian artery reconstruction, which all had good long term patency. In conclusion, proximal subclavian aneurysms

are degenerative in nature, while distal subclavian aneurysms are related to thoracic outlet syndrome. Management of proximal aneurysms is complex and commonly involves repair of concomitant arch pathology, while management of distal aneurysms must include a thorough evaluation and treatment of the thoracic outlet.

Given the rarity of the disease and the multitude of treatment options, literature regarding outcomes is yet to be well defined. Form the current literature, it does appear repair can be done from either an endovascular, open, or hybrid approach. Thank you.

- [Prof. Laurent] Thank you very much for giving me the privilege to present here this series. So that I don't have any disclosures. The definition of the aneurysm is there, you can see that there's three segments in which the aneurysm can be developed and these three segments are differs for their protological approach.

The aneurysms limits are best depicted by the dimensional imagery as you can see here. The aneurysms are really different according to their etiology the most frequent are

Atherosclerotic aneurysms, accounting for about 50% of the aneurysms and then you can have Dysplastic aneurysms accounting for about 20% which are very different in their morphology as you can see there. There's a neuro, you can see that this kind of aneurysm

is very difficult to be treated by endovascular procedures. Dysplastic aneurysms can be huge aneurysms. The Posttraumatic aneurysms account for about 20% or so, just like Spontaneous dissecting aneurysms are quite rare, it's about 2% only.

It's a very rare situation, only occurring in young patients finally. Unfrequent causes includes Mycotic aneurysms, Takayasu Disease or Becet's Disease, or other congenital origin or connective tissue disorders. The clinical presentation of the aneurysms

they are almost symptomatic only in about 80% either because of central symptoms or isolated local symptoms. The surgical approach differs according to the segment in which the aneurysm is developed. Of course the segments one and two are easily assessed

and the segment three needs a two team approach with neuroradiologist, which will do the access and going into the bone and the base of the skull finally. The open method you can approach the carotid artery you can be able to make an arterial reconstruction

in more than 80% of the patients either with graft-resection or with reconstructive aneurysmorrhaphy. The ligation occurs in less than 10% and should be mandatory associated with anticoagulation therapy. This is a new story called cervico petrous. From the beginning we were able to care for

and you can see that there were almost 20% of aneurysms occurring in this segment three, and the rest in segment one and two. These accounted for about 60 aneurysms. In the 61 operations, we made as you can see in the table

most of the time, bypasses with the great saphenous vein the superficial femoral artery or E-P-T-F and finally only nine resection-sutures. The mean clamping time for this patient was 46 minutes, and there were only seven ligation. Mortality rates, 3.2% including one patient who had

very large reconstruction of Takayasu Disease creating a thoracic arch on approach. The mortality and stroke rate is 8% or so. The late results are quite excellent, mostly seen here, you can see the Acturial survival was good because they were young patients.

The Peripheral and local sequelae was rare and the patency rates were excellent. The freedom from ipsilateral neurologic symptoms was excellent also. So what would you expect from endovascular therapy, which has been described with occlusive balloons,

coils, flow diverting stents and stent-grafts or bare metal stents, probably there can be room for this but there are several issues. First, the level of the aneurysm and the length of stented segment is to be considered. The Distal internal carotid artery is fragile

and a small diameter there can be usually intrasaccular thrombus in such aneurysms, kinks and tortuosities. And finally, I think that for low aneurysms in the carotid artery it's not necessary to have stent. In the aneurysms coming from the bifurcation it's

not necessary to have stents and probably the main reason to have a stent is for I located an aneurysm just like here but you can see that in this publication there was a risk to notice at the base of the stent so it can be an issue. And probably the hybrid surgery will go with

further progress in this kind of surgery because you can imagine having a stent at the base of the skull like this, and the stent can come here and overcome all the difficulties for kinking and tortuosities like this by an approach, a surgical approach of the carotid artery.

And if you go further you can imagine that we can have a hybrid surgery with approximate disease and this starts stenting off the aneurysm and the carotid artery. So in conclusion, this is a rare disease. Revascularization is performed in more than 80%

it provides excellent results. Surgical issues directly related to location and the role of endovascular and hybrid procedures, especially for segment two and three, should be established by further studies. Thank you very much.

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