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New In Vitro System For Evaluating Optimal Techniques, Main And Branch Endografts, Sizing, Etc. For Ch/EVAR: How It Will Improve Results And Decrease Complications By Leading To Standardized Techniques And Endograft Components
New In Vitro System For Evaluating Optimal Techniques, Main And Branch Endografts, Sizing, Etc. For Ch/EVAR: How It Will Improve Results And Decrease Complications By Leading To Standardized Techniques And Endograft Components
abdominalable covered stent (Advanta V12anatomyaneurysmanterioraorticballoonBalloon Expballoon expandablebehaviorcentersCHchimneyCordiscovereddevicedevicesendovascularEndurantevaluateevarexpandableexpansionforcegraftheterogeneityicastimpactMaquetMedtronicmitralniceoversizingpatencypercentposteriorproximalradialrenalscanstentStent graftstent graft systemStent graft system (INCRAFTstentssuboptimaltechniquetherapeuticversusviabahn
Pudendal Angioplasty (PTA) For Erectile Dysfunction: How To Diagnose It To Optimize Results Of Treatment
Pudendal Angioplasty (PTA) For Erectile Dysfunction: How To Diagnose It To Optimize Results Of Treatment
Non-Interventional Management Of CLTI: With Optimal Medical Treatment And Good Wound Care Many Amputations Can Be Prevented: When Is It The Best And Most Cost Effective Treatment
Non-Interventional Management Of CLTI: With Optimal Medical Treatment And Good Wound Care Many Amputations Can Be Prevented: When Is It The Best And Most Cost Effective Treatment
BKAcareendovascularhealhemodynamicischemiaischemiclimblowmultiplepatientpatientspredictproceduresrevascularizationSFA/PTA StentingVeithwound
DEBATE: There Is A Future For Stem Cell Technology For Treating CLTI: What Does It Depend On
DEBATE: There Is A Future For Stem Cell Technology For Treating CLTI: What Does It Depend On
DEBATE: There Is No Future For Stem Cell Technology To Treat CLTI: Sequential Compression Is Better And Cheaper And Beats Revascularization In Some Cases
DEBATE: There Is No Future For Stem Cell Technology To Treat CLTI: Sequential Compression Is Better And Cheaper And Beats Revascularization In Some Cases
ACI MedicalamputationARTASSISTArterial assist devicecapillarycellclinicaldiabetesfailedfailureimpendinginterventionlimbpatientsperipheralskeletalstemtherapeutictreatmenttrials
Update On Arterial Reconstructions With Bioengineered Vascular Grafts: How Well Are They Working
Update On Arterial Reconstructions With Bioengineered Vascular Grafts: How Well Are They Working
Why All DCBs Are Not The Same: Underlying Material Differences Are Important: Some Thoughts About Differences Between In.Pact, Lutonix, Stellarex, Ranger, Etc. And How They May Matter
Why All DCBs Are Not The Same: Underlying Material Differences Are Important: Some Thoughts About Differences Between In.Pact, Lutonix, Stellarex, Ranger, Etc. And How They May Matter
balloonballoonsBARDcoatedcoatingdosedrugDrug coated balloon catheterefficacyformulationINPACT Admiral (Medtronic)lossLutonixpaclitaxelparticlesproliferationpropertiesRanger (Boston Scientific)reflectedretainedsmoothStellarex (Spectranetics)therapeutictransfertransferreduptakevesselwall
Proper Hydration And Supplemental Oral Protein Administration Improves All Lower Extremity Ischemic Symptoms: It May Replace Stenting And Bypasses For Many Patients: The Evidence
Proper Hydration And Supplemental Oral Protein Administration Improves All Lower Extremity Ischemic Symptoms: It May Replace Stenting And Bypasses For Many Patients: The Evidence
"Coral reef" AortaangioplastyankleatrialAxilo-bifemoral bypassbrachialclaudicationcollateralscutaneousdecreasedehydrationdiarrheadistanceelderlyendovascularhydrationhyponatremiaiatrogenicintestinallesionslitersmedicalnatriureticoccludedocclusionpainpatientpatientspilotproteinrenalsensationspecialtystentingsubjectivetemperaturetreatmentwaterwith oclusion at the level of the diaphragm
A New Computer Controlled Balloon Catheter To Improve Treatment For Cardiac Arrest And Massive Bleeding: How Does It Work And Results
A New Computer Controlled Balloon Catheter To Improve Treatment For Cardiac Arrest And Massive Bleeding: How Does It Work And Results
Update On GraftWorx Implantable Piezoelectric Sensors For Remotely Measuring Vascular Graft And Stent Flows And Other Parameters: When Will They Be Available
Update On GraftWorx Implantable Piezoelectric Sensors For Remotely Measuring Vascular Graft And Stent Flows And Other Parameters: When Will They Be Available
acquireangioangioplastybloodcarotidclinicalconceptdatadetectdetectiondeviceDialysisexternalFistulafistulogramfistulogramsflowfluidgenerateGraftWorxhematocrithemoglobinImplantable Piezoelectric SensorsocclusionovinepatientsphysiologicproximalpulsatilesensorsensorsstenosisTransonictrial
New Developments in Coronary Evaluation by Non-invasive FFRCT
New Developments in Coronary Evaluation by Non-invasive FFRCT
agatstonanestheticangiogramangiographyasymptomaticcalcificationcalciumcardiacchestcoronarydeterminediseaseelectiveextensiveFemoro-popliteal bypassffrflowfractional flowhemodynamicallyischemiaischemiclimbmedicaremortalitypatientpatientsperipheralpreoperativeprevalenceproximalreserverevascularizationrigascoresevereSFA Occlusionsilentstenosissurgeryundergounderwentvascular

- Thank you very much for the nice introduction for the privilege to start the aortic session with this nice, very interesting topic about Chimney technique and especially about the in-vitro testing which we have done in Muenster in Germany. So, the Chimney endovascular technique we treat short necks as we see here.

With the use of off-the-shelf devices and the placement is in parallel and outside configuration of the main abdominal device. Well, if you see the literature we can see enthusiastic reports with the use of these alternative therapeutic options,

showing low incidence of endo leaks, excellent patency, and durability of these endovascular solutions. On the other side we have also centers with suboptimal experience, as we see here from Manchester, in the titled already publication,

late ruptures after single chimneys or from the group from Florida, highlight that the technique raises cause for concern. So what are the reasons for these divergent experience? Could be the heterogeneity of the used materials, but also the degree of oversizing

of the aortic stent graft? In order to evaluate that, we performed first of all a chimney case of a patient with a huge paraanastomotic aneurysm which we did with single chimney for the right renal artery, as we see here.

What we have done is the CT scan of these patients, we send to a special company and create this silicone model one by one with the anatomy of this treated case, as we see here, having a diameter of 28 millimeter, exact the anatomy of the renals,

of the neck length, infrarenally. And it was also really nice the opportunity to have a fluid simulation system, and we can have also the possibility to bring the device in the CT scan, and perform CT angiography, as we can see here,

very nicely the pictail catheter into the descending aorta, and evaluating now the impact of the different devices for this technique. Here is the example with the device you see here how we deploy the chimney graft, here is an Incraft stent graft for the right renal artery.

The first attempt was to evaluate the impact of different abdominal devices. If we use the same chimney graft in this particular case, the Icast for Advanta V12, and you see what we changed was only the type of the stent graft of the aorta.

If you see here the CT scan analysis, you see very nicely these combination of a mitral endoskeleton of the enduring device with a rigid, but very good, intraradial force Advanta V12, or Icast. You can see here how nicely performs

around the chimney graft. And if we see also in the reconstruction, we have a very nice expansion of the chimney graft, especially in the proximal edge, which is very important in order to have a good patency over the time.

You see here very nicely the expansion of the proximal edge of the balloon expandable covered stent Let's see now what happened with the Incraft. Again, you see here very nice the radial force of the Icast is here very nice to see. However, we have seen a completely different behavior

of the abdominal stent graft of this company. You see here that we have potentially more gutters compared to the other conformability of the endurant around the chimney graft. So it was a very nice sign and finding and showing the impact of the abdominal stent graft

for this technique. What we have done after that was we took the endurant device and we changed now the use of the chimney graft, so we used in the first attempt the self-expanding covered stents, the Viabahn,

versus a balloon expandable covered stent like the Begraft. And if you see here the results, you see again a very nice expansion of the endurant around the chimney graft, but in the reconstruction you see here the severe compression of the Viabahn self-expanding stent

has poor radial force despite that we lined we had per se 70 percent stenosis. I think it's a very important finding crucial compared to the balloon expandable chimney grafts you see here the Begraft, they had also a very good expansion

as balloon-expandable covered did, but also we see here completely different area of gutters if we compare the two balloon expandable covered stents in the anterior and posterior phase, you see here the Begraft plus seems to perform better. The impact of degree of oversizing we know

from the work of Riambaud 30 percent is the recommendation if you see this very nice analysis, you see here with 15 percent oversizing, we have this area of gutter versus 30 percent of oversizing you see a very nice conformability around the chimney that we chose how important is for this technique

to have enough fabric material to wrap up the chimney grafts. In conclusion, ladies and gentlemen, we have seen in this very nice in-vitro testing that indeed the area of the gutters vary depending on the different device combinations.

And also we have seen how important is the appropriate device selection, and 30 percent oversizing to obtain optimal results. Thank you very much.

- So I'm going to talk a little bit how to diagnose to optimize results in treating ED patients. I have nothing to disclose. What is erectile dysfunction? It is defined as the inability to achieve or maintain penile erection for satisfying sexual intercourse. The best tool we have to assess and diagnosis

it is the International Index of Erectile Dysfunction, which is a questionnaire, consisting of 15 questions, and a cut-off of 21 points was shown to be very sensitive to differentiate healthy individuals from patients suffering from erectile dysfunction. What the is the aetiology of erectile dysfunction?

We see here about 40% of patients suffer from a vascular problem, leading to erectile dysfunction. Whereas the other 50-60% of patients show multiple reasons for erectile dysfunction. So not surprisingly up to 50% of patients do show a suboptimal response to PDE-inhibitors Viagra therapy.

What is the pathophysiology of erectile dysfunction, coronary artery disease, and peripheral artery disease? They all show the common cardiovascular risk factors as we know them, and not surprisingly, erectile dysfunction was shown in studies to be an independent predictor of PAD and CAD

especially in the young male. And it was also shown that increasing severity of ED was associated with an increasing prevalence of peripheral artery disease. So in ED patients, screening, prevention, and therapy of cardiovascular risk factors and diseases

is very important. Here an algorithm I want to show with you or discuss with you a little bit more in detail. So if we have an individual with suspected ED, based on the IIEF questionnaire, the first thing we need to differentiate,

does this man suffer from a psychological ED problem, or from a functional ED problem? This can be answered by questions like does the patient have nocturnal erections that can also be objectively assessed. And once we think that the patient suffers

from functional ED, because he doesn't have any erections, then we need to differentiate, does he have an arterial underlying problem or a venous underlying problem? For that purpose, we can perform ultrasound examination. I will show you that in my next slide in more detail.

And pathologic or (mumbles) for an arterial problem is low systolic velocities, lower than 30 cm/sec and also a lowered resistance index, smaller than 0.8. There is a high end-diastolic velocity, may be an indication for venous underlying problem. So once we think we have a venous problem,

we can confirm venous leakage by dynamic cavernosometry or cavernosonography. And once we have identified the leaking vein this can be embolized or surgically ligated. If we think we have an arterial underlying problem we usually perform a CTA or MR.

This to differentiate from micro and macroangiopathy. Microangiopathy is every underlying arterial problem distal to the pudendal artery, leading to ED. And if we have a macroangiopathy, but only the macroangiopathy, PTA can be considered. So ultrasound examination, how is that performed?

We inject prostaglandins into the corpora cavernosa and then the penile artery is examined by ultrasound. Here is the flow pattern. So this is the end-diastolic. We need to assess the RR and the peak systolic velocities. So ultrasound is very important to rule out

an underlying venous leakage. But even if we have identified a patient with arterial ED problems, we are not at the end yet. We have studies from POBA studies and there was shown that we deal very frequently with the problem of recoil leading to re-stenosis, but also drug-eluding stents

were associated with patency rates of only 50-70% at six months. So over 40% of patients do not benefit after PTA at all. And this may be because up to 80% we think of patients presenting with functional ED do not suffer only from an isolated arterial,

but also from a venogenic problem. In summary, ED is frequently a vascular cause. ED is an important marker of cardiovascular diseases and proper anamnesis and non-invasive workup are very important to exclude ED from other causes, and especially concomittant venous leakage.

Thank you very much.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thank you very much.

- If someone asks me will the stem cell be effective for the treatment of for CLI in the future my answer will be definitely, yes it will be. Currently, more than 1200 cases of clinical trials using stem cells were performed in the world. In Korea we are now doing

more than 70 cases of clinical trials using stem cells. And as you can see in this world map, these clinical trials are performed widely in the world, especially the mesenchymal stem cells, was the main stem cells for this clinical trials.

This is a dog ischemic remoder. We encircled the femoral artery with a extracapsular ring, for constructing the chronic ischemic remoder and here you can see the abundant of criator vessels in stem cell treated rim compared to the counter rims.

This is a mouse ischemically motor. This model is most commonly used for animal study. This model can be made adjust on ligation of femoral artery. After those stem cell retreat, we evade with rim salvage rates

and also we can evarate the tissue necrosis. And we found there is a high link of rim salvaging in stem cell treated rims compared to the counter rims. This is a human clinical trial using stem cells. Picture A, C, E is a pressed stem cell angiogram.

And B, D, F is post stem cell angiogram of each patient. Look at picture E and F, compared to the E pressed stem cell angiogram. Picture F post stem cell angiogram here you can see the abundant of newly developed criator vessels.

We analyzed this 78 limbs of Buerger's Disease autologous with whole bone marrow stem cell transplantation. This slide shows the number of mono nuclear cells and the CD 34 (in audible 02:12) in parablood and bone marrow.

There are about 3 by 10 seven's number of mononuclear cells and the full count of Phibbs number will say they start at 45 themselves in one million (inaudible 02:25) bone marrow stem cells. We injected 30 (inaudible 02:29) or whole bone marrow stem cells in one

(inaudible 02:33) and this slide shows the result of the change ischemic pain score. As we can see here the ischemic pain score decreased after stem cell therapy. The degrees and rates of ischemic pain score was statistically significant.

As we can see in this right pain free walking time was also increased after stem cell treatment. This increasing rate was statistically significant. These outcome indicates improvement of quality of life according to the patient.

But the ankle brachial index was not increased after stem cell therapy. The difference was not significant difference between pre treatment and post treatment. But in toe brachial index, toe brachial index was improved after stem sell therapy.

This increase in rate in 6 months was statistically significant. This slide shows the proportion of change of ischemic score in pressed stem cell state, 70 percent of patients who are classified as category, 30 percent has category five.

This proportion of category shift to the category one to three after stem cell therapy. This resort to such as that stem cell therapy provided clinical improvement. So, what will be your choice for (inaudible 04:03) this is the future. Surgery or intubation,

but the stem cell just only using single injection. So, ladies and gentleman, today's ... my take home messages there is a future for stem cell technology for ischemic visceral therapy. Thank you for your attention.

- There is no future for stem cell. That's my disclosure (mumbles). That movie is taken from a secret facility on the 5th Avenue where they are doing human cloning. And as you can see that this is the operations that have harbored the human cloning. They are cutting the umbilical cord, and they're opening

the amniotic sac to deliver a baby who's a 40-years old male. Mental roduced as a spare part for a kidney, a heart, a lung, arterial system (mumbles), pancreas, you name it.

Primary amputation haven't change over the past decade. The only things that has been changing is the pixelation of the camera. We're still doing this very bad surgery. It's a disaster for the patient, for his family, for the nursing staff, for the treating physician

and for the tax payer money. We have a very aggressive policy of revascularization. We go any place that we are intended to go. We have no problem and we think we're doing great job. We could open anything, but does the patient benefit from such an intervention?

Its remain to be seen. In a very important publication last week the S-V-S objective performance goal, and it was a catastrophe for anybody who doesn't do a bypass. 30 Day amputation rate was doubled for bypass and tripled for endovascular.

Infra-popliteal Disease is stronger predictor of major adverse limb events than advanced age and tissue loss. Infra-popliteal endo-option is risky and harmful, and I refer back to our colleague in the cardiology and intervention radiology, because he could go for jail for that.

Had failed to meet S-V-S objective performance goal in any sort of category. After any successful revascularization, it can be wind up with Stenosis, Occlusion or total failure, without a recognizable persuading component. Despite this perceived failure, the limb can be

salvaged even in the absence of direct in-line flow to the outflow vessels. This fosters the wariness that there are further processes at play with neovascularization and ischaemic skeletal muscle paracrine effect. The stem cell failure establish a proof of principle

that therapeutic angiogenesis is regarded as a method of treatment for no-option patients suffering from C-L-I, however it did not reach its zenith. Preclinical studies spectacular efficiency of angiogenic therapy wasn't translated into clinical expected results. Critical appraisal of the stem cell, and what we find that

stem cells have failed totally, and moreover, is still in its infancy and there is many questions to be answered before we can hope that this treatment option would provide acceptable clinical outcome and sustainable results. This is the major three stem cell trials across, and it's believed larger than fact.

And it was discover that multivariate analysis exposed severity of rest pain, failed bypass, hemodialysis and diabetes as negative prognostic factors for amputation free survival. Any stem cell doesn't increase A-B-I in C-L-I patients, even with repeated administration.

Critically ill patients with gangrene and impending amputation did not derive any benefit and it is totally ineffective in elderly patients. Moreover, that's Francis Moll's advance trial. After a couple of billion dollars, placebo effect is as good as stem cell therapy.

Stem cell based therapies failed to deliver and clinical results have been disappointing. None of the current trials have shown any improvement. Advanced therapy by manipulation of capillary network have to be given a chance. Sarcopenia develop capillary bed failure and contraindicate

any form of any intervention. We have to understand why a lot of claudicant don't progress to C-L-I and vice versa. And we have to understand more about pathophysiology of skeletal muscle in C-L-I and the mitochondria failure. And the effect of sarcopenia, smoker and diabetes

on the C-L-I. And we have to think laterally about capillary bed recruitment. We use the ArtAssist, which work on the principle of forced emptying of capacitance vessels, thereby increasing arterio-venous pressure gradient and lead to increase in

perfusion pressure who otherwise would be at impending risk of limb loss and are amputation bound. It promote healing and improve limb salvage in when revascularization options are unavailable or exhausted and when established treatment alternatives are lacking. It increases arterial-venous pressure gradient, it reduce

peripheral resistance, reduce white cell damage, increase collateralization and sheer thinning. We have more than 18,000 referred, 12% had C-L-I, 41% had intervention and 18% had (mumbles) therapy. 41% were not fit for intervention and 10% had prior amputations, however 583 out of 620 used the home

ArtAssist for 90 days, and 47 used if for more than 150 days. We witnessed C-L-I patients with haemodynamic clinical improvement from Fontaine Grade five and six to grade three, after 90 days. Programme was designed to control acute C-L-I symptoms

and improve general condition of patients prior to any revascularization. However, at the end of the 90 days, C-L-I patients did not require any interventions, ischaemic ulcer healed and there was no need for any pain medication as home therapy.

Ladies and gentlemen, Mr Chairman, the clinical efficacy of ArtAssist imparts essential benefit and a worthwhile non-operative option to patients who otherwise would be at impending risk of limb loss and are amputation bound. ArtAssist has superior limb salvage, ameliorated amputation

free survival and provides rapid relief of rest pain without any intervention in patients living on borrowed time. We must acknowledge the limits of stand-alone intervention, capillary bed recruitment avoid fiascos of surgical, endovascular or cell therapy. It reduces peripheral resistance and enhance

endothelial function. Augments clinical outcomes of otherwise failure bound good interventions. Thank you so much for the opportunity to present our work in New York.

- I'm going to try to give you a brief update of what we've been working on for 20 years which is tissue engineering human blood vessels. By disclosure, I currently serve as chief executive officer for Humacyte which is the company that's developing these blood vessels and are in phase three clinical trials.

We've been trying to actually engineer human tissue in the shape of a blood vessel for about 20 years and have made considerable progress. I'll tell you we've now finished enrolling the phase three clinical trial for hemodialysis access and have advanced studies for

peripheral arterial reconstruction and civilian trauma. The way we make these blood vessels is we actually place them, human vascular smooth muscle cells, on on a biodegradable scaffold made of polyglycolic acid. They're grown in what we call three dimensional culture for actually about eight to ten weeks

to grow the cells to confluence to make a human vascularized tube or vessel. To make them commercially available, ultimately, we now take banked cells from actually organ donors where we collect large volumes of vascular smooth muscle cells from the descending thoracic aorta.

We grow them in bioreactor bags, actually, we've now scaled this to be able to make 200 of them at a time and we'll have the capability to produce, literally, thousands of them per year. To make them universally implantable,

the donor antigens are removed and we have an acellular human tissue that then can be delivered to operating rooms in sterile conditions and be available for immediate deployment in vascular trauma or peripheral arterial disease.

This is actually what it looks like histologically. This is a cross section of the vessel here stained for type one collagen, type 3 collagen, fibronectin, vitronectin. We know there's a number of other proteins that are in the matrix that are left

by the cells that manufacture this vascular tube. They are low abundance proteins that drive the remodeling process once implanted. This is actually what it looks like if you're a surgeon. It specs out our current commercial or clinical platform as 42 centimeters long, 6 millimeters in diameter.

It's got suture retention and burst strength that are commensurate with human saphenous vein and human mammary artery and as you can see in the lower panel it's got handle attributes that where you can tunnel it in multiple different configurations for both AV access

as well as arterial reconstruction. This is what an explant looks like. You can see it doesn't have an encapsulated, so a foreign body reaction, which we see with conventional synthetic materials, it's got what really appears to be

the development of an adventitia and I'll show you some confocal microscopy in a second from a human explant that actually has evidence of capillary ingrowth and endothelialization. If you take one of these vessels and in this case implant it.

It's the acellular structure, as I mentioned, there in cross section, and once implanted it repopulates with vascular smooth muscle cells from the recipient. You can see stained in brown for alpha actin and the evidence of capillary infiltration

or angiogenesis into the media of the vessel and you can see the vessel actually reline with endothelial cells. So while we've manufactured human tissues in acellular structure once implanted it develops the attributes of the hosts'

own blood vessel from the hosts' own cells. We've now done extensive clinical implants in patients, actually, our first human implant was in 2012 in dialysis access. We've been able to demonstrate enduring patency as illustrated by these red bars

over 24 months for our AV access program and have been able to demonstrate really a freedom of infection and the ability for the vessels to heal and remodel. This is confocal microscopy from a human explant and you can see the media of the implanted vessel

here stained for vascular smooth muscle cells. The adventitia with evidence of capillary ingrowth and an endothelial cell lining of the vessel when implanted. We've also been able to demonstrate that the tissue has the capacity to heal which is in contradistinction to PTFE

or synthetic materials in the lower panel but you can see over time, this is from again a dialysis patient, but a cannulation injury. This is a previous needle cannulation, an evidence of the tissue to actually heal and remodel.

We've now done extensive arterial studies. Our first arterial implant was in 2013. This is an example, of a common femoral artery bypass to a popliteal artery and you can see in the angiogram here, in this case, six months after implant of the bypass in a lower extremity fem pop.

With the support of the US military, we've now initiated civilian trauma studies, where we've been able to bypass femoral artery injuries in the lower extremity in a number of patients with both gunshots and traumatic injuries to their femoral vessels and have re-initiated

a small caliber program for coronary artery bypass grafting and will be, ideally initiating pediatric congenital heart surgery Blalock-Taussig shunts, within the next year. So in summary, off the shelf bioengineered blood vessels are possible.

We've been making them now for a number of years. They appear to be non-immunogenic, integrate with native tissues, repopulate and remodel. Post implant, they actually increase with strength because the host actually incorporates their own collagen once implanted.

Phase two clinical studies are complete in hemodialysis access and ongoing for peripheral arterial disease and global phase three clinical trials for hemodialysis have just completed enrollment and a number of arterial programs are in development.

Thank you.

- Basically, what I'm going to try to tell you in the next few minutes is that DCB balloons are indeed not all the same, and will try to explain you why this is the case. This is a list of DCB balloons which are currently available on the market or in pre-market phase.

They have all one thing in common. They all using paclitaxel as the drug. As for the rest, however, all these devices differ. They differ in the dose that's supplied. They differ in formulation of the paclitaxel. They differ in the excipient that's used.

They differ in the balloon properties and the coating method. What are the important factors for DCB to be efficient, to have that biological effect? Well, first of all, there has to be the antiproliferative agent, of course,

which is paclitaxel. Paclitaxel alone is not enough. There are differences in the way the paclitaxel is applied to the balloon, in the dose and formulation, and in the binding on the balloon surface.

The balloon end has to be transferred from the package to the lesion, and a lot of the drug is lost during the transfer process. Some particulars are embolized and these kind of systemic effects, which of course, are important.

Then the drug has to be transferred to the tissue itself, and that too, is a process where the coating characteristics, the excipient, and the coating techniques can make the efficiency of that transfer process different. And a loss of paclitaxel,

which is in the vessel wall history exerted function on the proliferation of the smooth muscle cells and to the homogenicity of distribution and the solubility of paclitaxel can be important factors. The first factor in it was the formulation of the paclitaxel

and you see paclitaxel is not paclitaxel, paclitaxel in crystalline formulation is different from or has different properties from an amorphous formulation. As you can see here, it's easier to release the particles when they're in crystalline form,

but they are better retained over time in the vessel wall. This is reflected in the actual concentration of paclitaxel, which can be found in vessel wall shown in this study. The coating techniques still evaluate and the new techniques, such as nano-encapsulation, are being used in some of the new DCB balloons.

The integrity of the coating is different from balloon to balloon, too. Here you see a simple simulated shake test. You see that there are more particles coming off from some of the balloons than from others. This is reflected in the loss of balloon

during the transfer progress. This, probably, is one of the reasons why for instance, the IN.PACT balloon a higher dose is needed than with other balloons in order to have the same vessel uptake in the wall. The shake off test is one test during hydration,

during the transfers through the bloodstream, things change with the coating also has been illustrated here. This can result in the loss of particles during this transfer. The particles which are found back downstream.

In this one study we compare three of the most used different drug coated balloons. It's showing that indeed this embolization can be different, or the number of particles can be found distally can be different.

However, not only the number of particles is important, also the size of the particles. As you know, the obstruction of the capillaries and small blood vessels can be, might be an issue or concern in this use of drug coated balloons.

The excipient is very important factor, which supports the uptake of the drug by the vessel tissue. It acts as a molecular spacer to increase paclitaxel's surface exposure and facilitates a transfer to its hydrophylic properties. The excipient is important.

We know this already from the very beginning of drug coated balloons. The first drug coated balloons which were used without the excipient actually proved that to be efficient. The excipients also differ in properties,

as you can see here. These are two very early used excipients, lopromide and urea. You see they differ in the efficacy to retain the drug on the balloon, as far as in the transfer of the drug itself.

The excipient and dose density can also be used to tune the coating durability, as can be seen in this experiment. What also happens in vessel wall? The transfer of paclitaxel into the tissue, of the storage of the tissue,

occurs in the solid phase. In that solid phase, this is the way it's retained in the wall. It has to be retained there for certain time in order to be efficient in the, to avoid proliferation of the smooth muscle cells.

You see that this, the way it is transferred into the vessel wall and stored in the vessel wall, is not a very important factor which will determine the long term efficacy of the paclitaxel, the final efficacy in doing what it has to do,

as can be seen in this experiment. This is reflected in the pharmacokinetics of the presence of the drug into the vessel wall and thereby to its long term efficacy. Last, the balloons also differ with regard to their other properties.

Some have no 14 platform or 35, and in the sizes which are available. As a conclusion Mr. Chairman, I think we can say that unlike simple angioplasty balloons, DCB's are not purely mechanical devices,

but sophisticated materials that have to transfer direct from the package to the vessel wall. The dose formulation, the surface properties of the balloon, the coating process, and the excipient all have their influence on drug availability

in the vessel wall, on its efficacy, and on the results. Individual properties of the balloon will be reflected by these properties. Therefore, DCB's are certainly not all the same. I thank you for your attention.

- Thank you Ken. I have no disclosure. The medical treatment of claudication and rest pain includes suppression of tobacco, supervised exercise, cilostazol, and control of risk factors. We had a number of patients who failed to the medical treatment.

One of them is this lady, who was an 84 year old, a heavy smoker, had two MIs, who came claudication to, a 10 step claudication, intestinal angina, and renal insufficiency, and she happened to have an occlusion of the aorta and she was not a surgical candidate

and we couldn't pass any wire. So, what we did is ax-bifem. She did very well. And, but after three months she came back with the same symptoms. We thought that the bypass was occluded but it wasn't.

And the patient had had diarrhea for five days. So we hydrated this patient. After the second day she was not having angina and she was able to walk without any limits. The second patient we had was asking for an amputation after four bypasses and several treatment,

endovascular treatment, and one of my partner and I ask him to, asked me to take care of him because he was drinking less than 700 CCs a day of water. So he put the patient on two and a half liters a day and in two days the patient had no pain and after one years he's walking four kilometers

with the only treatment of water. So, obviously that caught our attention because after so many years of doing this specialty we have never seen these at this level. So, the common factor in both patients were dehydration, was dehydration.

So, we organized a pilot study, a prospective trial with patients with claudication and rest pain or lesions who did not respond to standard treatment. So we have the approval of the ethical committee and initially we started with 36 patient who accepted to sign the pilot study

for, to be included. So, the medical treatment continued but we were giving two and a half liters of water a day and three grams of salt and, so, we were measuring the ankle brachial index. We were putting patient to treadmill

and calculating the time and distance to claudication. We were doing per cutaneous PO2 temperature and subjective pain (mumbles). We started with three liters and then with two liters. After six weeks and six months all tests were repeated and subjected to statistical analysis.

52 patients drunk two liters of water or more. All patients who complied with the protocol had a significant increase in the skin temperature and also ankle brachial pressure, distance to claudication, and decrease in pain sensation. This is after six weeks, the cutaneous temperature,

cutaneous temperature on the other foot. Distance to time to claudication, now this is amazing because they improve at least five times. And subjective pain sensation decreased. Ankle brachial index increased. What happened at six months?

These patients kept improving. That means that they were developing new collaterals because even stopping the hydration they had no pain. So, this is the ankle brachial index after six months. This is the pain index at six months. This is temperature of the foot at six months,

and distance to claudication. This is the most significant change we have seen. So, our patients are not receiving any medication, just water, and also we learned that those patients had a very low protein concentration. So we added protein to the water and salt

to prevent hyponatremia and even patients with lesions you can see that after four weeks this patient receiving no medication, no antibiotics, just local care and water, he was healing the lesions. Dehydration is common in elderly patients as you know. Dehydration can occur because fluid losses

or decreased intake. Elderly people drink less fluids because the sensation of thirsty decreases. This decrease can occur because of depletion of dopamine and increased level of plasma atrial natriuretic peptide. The body water composition decreases in the elderly

and because decrease the muscles and increase the fatty tissue the renal function is impaired with less capacity to concentrate, increasing urine formation. Kidneys are also less reactive to ADH and have a lower ability to regulate sodium excretion.

Last, iatrogenic factors can aggravate dehydration. Conclusion, most of the elderly patients with intermittent claudication were drinking a low volume of water, median one liter, most of them less than that. All patients responded to an increase of water intake. The difference in pain sensation, ankle brachial index,

and distance and time to claudication comparing before treatment and after treatment were statistically significant. In the last 12 months our cases of angioplasty or stenting dropped almost 90%, with a concern of the industry.

Thank you very much.

- Thank you for the kind introduction, and also one thank you to Dr. Frank Veith for inviting me to this meeting to talk about this. The disclosure is that it is not intended for human use in the US for the moment. Go back to the Colonel Carl Hughes in the Korean war. You know, this thing about the REBOA balloon

to help in traumas. We know that's its the 4th leading cause of death in Western countries and you can use a REBOA balloon for verified positioning and filling during the hemorrhage control. So there was a young doctor, he's still young, in Denmark,

who noticed that when he was on-duty that it was very difficult to help cardiac arrest people. He got the idea that maybe you could put in a REBOA balloon. That way when you do cardiac resuscitation, maybe you could (mumbles) the balloon and the blood will only go the coronary vessels and to the brain instead.

We know also that if this is going to be a thing that works well, it has to be maybe positioned and learned by paramedics, without having an angio-suite there. We know already that the world's first pre-hospital REBOA was performed by London Air Ambulance in June 2014.

And we also know that use of aortic occlusion balloon catheter without fluoroscopy for life-threatening post-partum hemorrhage has been in Norway, also in bigger studies, than in this. However, the procedure they suggest can also be performed by others and the endovascular specialists trained by

anesthesiologists and surgeons who are trained to the vascular access techniques in the future. The problem is that you have to put the balloon right and not into the renal vessels or even higher up. So what this balloon has been developed to do, it has a sensor computing and its patent with vascular

resuscitation or suspended state in cardiac arrest. It has redistribution of the cardiac output to increase supply to the brain and heart. And the sensor is follow of a predefined reaction pattern based on an electrical signal and its computer receive patient data which identifies physiological

and/or anatomical characteristics. So this is the way it was supposed to be. So let's see it works. During ongoing compressions the device go up just as normal as a REBOA balloon or aortic balloon and while doing the ongoing compressions the balloon is inflated

and electric signal goes to the computer on the outside. Also inflated just enough so it doesn't hurt the aortic valve or the vessels there. So that case the ongoing compressions that's the idea about it, it goes to the brain and the coronary vessels. So it has positioning feedback.

Its computer-assisted positioning feedback protects against inadvertent positioning inside vessels during occlusion with or without fluoroscopic guidance. Second it has an automatic filling and deflation and balloon pressure adjustment, to ensure a secure and soft occlusion, based on measured pressure

from beginning to the end of the procedure. And its built-in pressure safety mechanism protects against manual or automatic overinflation, rupture and unintended damage as compared to the REBOA field today. So in what we do now, we have done cadaver studies and we also have done pig studies

and we are analyzing the data. And we are just planning to have randomized control times in (mumbles) in Switzerland to have using these balloon or not for cardiac arrest to see what the future brings to this. This was all about the idea from a 24-year-old MD student

in Copenhagen who raised findings to this. And besides doing this, we also will also do an endovascular simulation training to give this out to paramedics in the future. That's our idea about this. Thank you.

- Thanks again, and thanks to Dr. Vieth for the kind invitation again this year. I am on the scientific advisory board for the device. So remotely monitoring flow in vascular structures is not a new concept, Dr. Vieth and colleagues actually reported this several years ago. But the technology has finally caught up with that concept.

So this device involves a microsensor which is a piezoelectric polymer, bluetooth technology to then wirelessly transmit this data for external processing. At this meeting in the past we've reported our initial in vitro results with the bench top model

showing the concept is possible on the bench top, both to determine degree of stenosis, and actually location of the stenosis, distal or proximal to the sensor. There's also in-vivo data in an animal model, an ovine carotid bypass model,

which shows the ability of the sensor to transmit through the tissue under physiologic conditions. We then use this to also show the ability of the sensor to detect stenosis and occlusion in an in-vivo ovine carotid model. Most recently, we've actually done a human

proof of concept trial in AV fistula patients, using an external patch containing the sensor and the transmitting equipment. Seventy six patients were studied, that were coming in to and angio suite for fistulograms and or angioplasty

for their fistula and their access, and measurements were taken at that time, both pre and post evaluation. We found 100% success, both in acquiring data and in storing this data remotely.

And the findings were actually corroborated by the fistulogram that was then performed. Eleven patients actually didn't have significant stenosis, and 65 had stenosis or occlusion, and you can see the data, which is generated by the device,

in the lower bars, showing both stenosis, on the left, and occlusion on the right, and juxtaAnastomotic stenosis of 75% in the lower blue bars. Additional sensors can be placed on the device. This can be done with new microsensors, which can be placed right next to the original sensor.

Phonoangiography can give volumetric flow rates, accelerometers can be placed, which can actually show thrills and pulse and generate acoustic data. Photplethysmography sensors can be placed, and thermal sensors can be placed

to generate such data as hematocrit, degree of stenosis, heart rate, possibly even blood pressure in the future. Some of these sensors have been placed, and there's a high correlation when they're used to Transsonic flow probes under pulsatile flow conditions

to show that we can actually generate information on flow, both peak and lack of peak, and it's very accurate in terms of its comparison to these Transonic flow probes. You can also detect hematocrit. So the sensor can actually be utilized to show

hematocrit in human blood samples with a strong correlation to standard measures of hematocrit and hemoglobin using the device. Detection of blood volume is also possible with these new added microsensors. There's peak detection of the photoacoustic spectrum,

which can allow a determination of total blood volume. So the concept is to acquire the raw data through whatever array of sensors are desired. Initially, right now, we're still using the piezoelectric sensor to really just monitor flow and stenosis.

Signal processing can then be performed using machine learning. This has actually being placed into the algorithm, so that machine learning can accumulate and analyze the data. For clinical metrics which can then be

acted upon by the clinician. There will be a trial beginning in 2019 in Europe, again utilizing an external patch sensor, and dialysis access patients to see if we can acquire real time, remotely monitored information, and then alert the clinicians appropriately to

predetermined clinical criteria. This is the current variation of the patch. It is worn for 7 days, is sweat and waterproof. It could actually be worn longer than that, but we're going to have the patients change the device after 7 days.

It's easy to apply, comfortable to wear, it does have this multi-modal sensor capacity. It can add up to ten sensors on the device to generate both optical, acoustic, thermal, and mechanical information, and it will automatically monitor the patient's dialysis

access over which it's placed. The battery life is 2-3 months, but we're going to change the patch, each one, after only seven days, so that won't be an issue. And you can automatically measure, you can actually generate as much data as you'd like,

but we're going to generate at least eight pings, or eight data acquisitions per day. So the real time fluid management is also possible with this device. You can actually utilize this to generate, hopefully, both flow information and

information on fluid volumes. So this is our timeline. We'll start the trial in 2019. We hope to have FDA approval for hematocrit, flow, stenosis, and cardiac output in Q1, Q1 and Q4 of 2020, and we look forward to

presenting the data at further meetings here in the future. Thank you very much.

- Thank you very much, I appreciate the opportunity to update you on non-invasive fractional flow reserve. And here's my disclosure. Non-invasive fractional flow reserve is a new cardiac diagnostic technique based on coronary CT scans.

It provides a three dimensional map of fractional flow reserve values throughout the coronary tree and values less that .8 are hemodynamically significant and indicate coronary ischemia. Now, this is now FDA cleared, reimbursed by Medicare

and private Insurance and is used clinically in patients with chest pain. However, it's not really been evaluated in patients without chest pain and more than 50% of patients who die suddenly or come in with acute MI do not have preceding coronary symptoms.

So, silent ischemia is a real issue and is a real issue for cardiovascular mortality. We certainly know that patients with peripheral vascular disease have coronary disease and this is very often unrecognized. The risk is particularly high at the time of surgery

and it's interesting that guidelines recommend no preoperative cardiac evaluation on patients without chest symptoms or coronary disease signs thus, we really don't know what the prevalence of silent coronary ischemia is in peripheral vascular patients. We do know that the highest risk

is in critical limb ischemia patients with 20% mortality in one year and 50% mortality in four years. The data I will show you today comes from a ongoing prospect of study headed by Professor Dainis Krienvins in Riga Latvia to determine what is the prevalence

of unsuspected hemodynamically significant coronary disease in peripheral vascular patients and to determine its potential benefit in the patient management. The first publication from this experience came out in September of this year

on vascular disease management. And this presented 54 patients with critical limb ischemia. These patients had no cardiac history, were cleared for revascularization surgery and normal EKGs and underwent pre-op of coronary CT and fractional flow reserve computation by protocol.

The first thing that comes an issue in peripheral vascular patients is calcification. Guidelines recommend that you should not do coronary CT if your calcium score is greater than 400. The average calcium score in this group of patients is greater than 1000.

And although CT accuracy in high calcium scores is not, is not great you can certainly do FFR computation. Interestingly, 9% of the patients had left main disease. And in here in this example, you see extensive coronary calcification with a right Agatston score of 3800 with a clearly hemodynamically significant lesion

in the left inter descending coronary artery. If we look at fracture flow reserve, it's remarkable that two thirds of the patients have severe coronary ischemia. This is silent ischemia. These are all asymptomatic patients.

Most of them have multi-vessel disease as seen on the right here. And some of them have isolated left single vessel disease. What's interesting is that the ischemia determine that an FFR value of .8, if it's less than .7 that is very severe ischemia and that was present

in 43% of the patients. So, what do you do with these patients now who are in for vascular surgery but have severe silent coronary ischemia? Well, according to the guidelines, you should operate on them.

And with vascular team guidance of anesthesiology, cardiac surgery, cardiology, most of the patients underwent their vascular surgery procedures just fine. 91% had vascular surgery, 5 were postponed, there were no post-operative deaths. Post-operatively, the patients had the elective coronary

angiography and coronary revascularization is appropriate. That was done in 30% of the patients. There's been no death or mortality or MACE events in 90 day follow up. Heres a case example of a patient 59 years old, severe right coronary stenosis.

You can see one month post op the end of a coronary angiography and elective coronary stenting. Here's a patient with multi-vessel disease, ischemic ulceration. You can see the extensive coronary calcification, the severe stenosis of the proximal right coronary artery,

which on the angiogram and now is treated six weeks post op with a stent. So, what do we learn from this experience? We, first of all, we see that patients who are undergoing elective peripheral vascular surgery have a very high incidence of unsuspected,

asymptomatic coronary ischemia. That doesn't mean they can't undergo their surgery. They do undergo their surgery successfully. We do that everyday. Patients almost never die on the operating table. And they survive their surgery

because of good anesthetic care. Whether they have improved long term survival with elective post operative coronary revascularization, that will require a longer term follow up to gather these data but I suspect you will probably see a beneficial outcome

from such treatment. Thank you for your attention.

- My question is to Dr. Neville. Is the sensor actually on the graft, or is it in that little patch? - [Dr. Neville] Well, in the current trial in Frankfurt that's going to be started in Europe in 100 patients, the sensor is in the patch. It's an external patch for this initial trial.

It can be placed on the graft. We've done that. We've done that in vivo in the animal trials, but the initial trial, just to show that there's proof of concept in these fistular patients will be in the patch.

- Will you ultimately have a sensor that's implantable on a stent? - [Dr. Neville] Yes. So, there's a prototype which has been developed already where the sensor can be placed on sort of a ribbon-like piece of piezoelectric material,

which can be wove between the struts of the stent, and it's been shown. We've deployed it already. There's no damage to the sensor on when the stent is deployed. - [Man] Wow.

Amazing. - [Man 2] Yeah, that's pretty great. - Thank you. I have a question for Professor Donus. I was interested to see the differences between the devices that you showed. What is it about the main bodies

of those devices or other devices that you studied that allows them to conform or non-conform? In other words, larger or smaller gutters. - Yeah, I think of the device of the skeleton is important.

We have, as you know, the Nightlander skeleton from the enduring device. We have a stainless steel endoskeleton from the Zenit platform. What we need for chimneys is to have a nice conformability between the abdominal stent graft

and the chimney graft, so it seems very important, the design of the skeleton and also the radial force of the chimney grafts. - How would you, if you were going to have an endograft that conformed very well for chimneys, how would you design that top ceiling stent?

- I don't like to say that to have the patent for that. (laughter) So probably it would be a combination of high radial force in the proximal edge and flexibility in the distal edge in order to feed those angulated renal arteries.

- [Man] Dr. Sultain, you have a comment. - Yeah, I'd like to comment on the finding of Dr. Zarens that the complication regarding MRI and ischemic problems post-intervention have dropped. That goes with the recent publication about the SBS goal of outcomes.

Show that we don't have any more cata complication. What we have more amputation and limb loss, whether you do an angioplasty or bypass, and this raises a big concern because we have done all assessment for the contemporary practice in the United States,

and we find that if you do an endo, you triple the risk of losing the leg rather than a bypass, so I don't know where we stand in here and whether that we have to talk to our colleague in cardio intervention radiology. Tell him that we need to do more bypasses

rather than angioplasty. I'd like the comments of the panel, please. - So, in critical limb ischemia patients, the endpoint is very interesting of, so, if you consider periprocedural mortality, I think that's right.

You don't have very much periprocedural mortality, but you have postprocedural mortality, and you have long-term survival, so in critical limb ischemia, the primary endpoint is usually amputation-free survival, so if you translate that in another way,

if the patient dies before you cut off the leg, your procedure worked, so in the long-term perspective, you really have to consider patient survival, and we generally ignore long-term survival as an endpoint in vascular procedures, but if you pay attention to the coronaries,

and you correct left-main stenosis, proximal LAD stenosis, really critical lesions that are there and are asymptomatic, you'll probably increase long-term survival. - [Man] I'd like to ask Dr. Prody a question. One, is there something in the water in Buenos Aires that is special, or have you tried adding it

to something like Gatorade? Any of those things seem to make any difference? - This is basic physiology. 80% of the arterials are uprooted because they are very strong with muscle. When you increase the fluid, if you take the patient,

the elder patient to Artisan, you will find that all of them have the femoral activa collapsed, and all of them, the intake of water is less than one liter, and we need more than two, so all the other population, most of them are dehydrated, so they have less circulating blood volume,

and as vascular surgeons, we always see what is outside but not what is inside, so when you increase the circulating volume, you have more flow coming to the arterials, and this is a physiological stimulus for the secretion of nitric oxide.

That dilates the artery, increases the resistance, and you have more fluid coming in, and as you know, 60% of the blood is stored in the veins, and when we give this patient two and a half liters of water and we do an ultrasound, the femoral activa is round instead of being collapsed

and the profusion of the limb increases. In the long term, the increased flow found in collaterals increased the size of the collaterals, and even if they stop drinking for two days, they don't have complication, and if you study those collaterals, they're much bigger

because through months, they had more flow, so this is physiologic basic knowledge, but most of them, we ignore this before. We need at least two liters a day, and most of our patients drink less than 700 ccs, and this is basic knowledge, and I think

in our experience, for us it was like a miracle because we were using 10 silver PTX a month. We are now using none, and we were doing a lot of distal bypasses, and now we're doing one or two a year, so even for us, it was a surprise, but it's a good surprise for the patients

and for Medicare who's going to spend much less money. - You know, our sensor can monitor blood volume. I'd like to put an external patch on all of Dr. Prody's patients, and we'll give him good feedback on their volume stats.

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