- I have nothing to disclose. So, just as a matter of background, you've heard a lot about catheter-directed thrombolysis as a means to improve RV function in patients with acute pulmonary embolism. I think there's a lot of limitations to a catheter-directed thrombolytic strategy,
including need for ICU stay for catheters, need for thrombolytics, which even at low dose do carry a finite risk of intracerebral hemorrhage, and other cost related issues. And so, again, to reiterate the last two speakers, a single session, non-lytic based therapy
that's definitive for pulmonary embolism certainly could have a lot of use. And so, I don't really need to outline the importance of the RV to LV ratio as a marker for high risk in pulmonary embolism other than to say that it is very difficult to do a randomized prospective
clinically blinded study in pulmonary embolism for this fact that in the submassive population we're used, unfortunately, used to having surrogate markers for clinical improvement, such as improvement in RV LV ratio. Nevertheless, it is a good outcome
in that it is very reproducible. CT scanning has been shown to be the best way to really get reproducible results with RV to LV ratio. I will talk about the FlowTriever System, which in its original design consisted of an aspiration catheter which is a 20 French catheter
directed from the femoral vein typically into the pulmonary arteries and then the FlowTriever Device which is these nitinol disks that can grasp the clot and help it withdraw and then the retraction aspiration system which is a manual suction based system to withdraw the nitinol frame
as well as to aspirate the clot. So, this procedure and device were studied in the FLARE Study. We wanted to evaluate the safety and efficacy of this device. We looked at 106 patients in 18 sites.
It was prospective single arm multi-center, and we looked at outcomes at 48 hours and 30 days, primarily looking at efficacy with the primary outcome being reduction in RV to LV ratio at 48 hours as well as safety which was a composite major adverse event rate, including device related death, major bleeding
according to the VARC-2 definition, as well as treatment related adverse events such as clinical deterioration, pulmonary vascular injury, cardiac injury, all of the things, the dreaded complications that we worry about when instrumenting these patients who are acutely ill.
We measured these outcomes at 48 hours and followed the data with the typical Data Safety Monitoring Board and Clinical Events Committee that were all independent. So, the inclusion criteria were typical patients aged 18 to 75.
They had to have evidence of proximal pulmonary embolism by CTA. Most of these patients would probably fit into what we would call an intermediate high risk by modern definition. We did exclude patients who were profoundly hypotensive,
patients that had evidence of perhaps chronic pulmonary embolism. They did have to have heart rates less than 130 as well. The exclusion criteria, we didn't want to blur the results with patients who had failed thrombolysis. So that was excluded.
We didn't want to have patients with severe pulmonary hypertension greater than 70, which perhaps might be an indication of chronic pulmonary embolism. Vasopressor requirements, people who had FiO2s greater than six liters per minute to keep their sats up, patients who were profoundly anemic,
patients who had recent cardiac or pulmonary surgery, as well as actively progressive cancer. Of note, patients with a high bleeding risk other than what I had mentioned were included in the trial. We had a very successful enrollment as you can see. We had 106 patients that were enrolled, one of which was
enrolled but unfortunately did not meet eligibility. She had undiagnosed metastatic breast cancer at the time of her enrollment, and so, that was the one patient that ended up resulting in a study related death. We had two patients who received thrombolytics adjunctively
as part of the procedure. That data was analyzed separately. So really the core of the patients were 104 patients who were treated only with the FlowTriever and did not get any adjunctive thrombolytics. As far as baseline characteristics,
we treated 106 patients. The average age was 55.6. The mean BMI was 36.1. I'm based in Louisville, Kentucky and that's below average for our BMI. But unfortunately, DVT and PE is a disease
of obesity, which is only increasing in this country. You had the typical other comorbidities including hypertension, coronary artery disease. 73 patients or 69% had concurrent DVT. Several patients had a history of prior DVT or a prior pulmonary embolism.
As far as the characteristics, we had sPESI score of one in about 45% of the patients, positive troponin in 60%, D-Dimer of 75%, elevated BNP in 73%. Most of these patients had bilateral pulmonary emboli. And as far as prior treatment, most of them got unfractionated heparin.
Some of them got low molecular weight heparin. Almost all of them had femoral access from the right. The other alternative access was from the left. We did not have any patients in this trial that were treated from the internal jugular approach, although that is possible with this procedure.
As far as the devices used, there were a mean of 1.7 devices. We had three sizes, small, medium, and large with an average number of passes of four passes for the treatment, a mean procedure time of one hour and 39 minutes ranging from 39 minutes up to three hours,
and we had zero technical complications in terms of success for delivery, deployment, or retraction of the disks. Here's the example of the delivery of the catheter. You can see in real the advancement of a 20 French catheter from the femoral venous approach over a stiff guide wire into the pulmonary artery.
So, as far as delivery this proved to be quite technically successful and feasible. You can now see that the FlowTriever disks are deployed within the pulmonary artery. You can see that there are two disks deployed. One disk remains retracted into the aspiration guide
catheter and it turns out for our technical point that was the most important thing was to place the aspiration guide catheter close to the clot and then you can see examples of the type of clot removed here. As far as the main efficacy outcome we had
a decrease in the RV LV ratio from 1.5 at baseline to 1.15 with a reduction of .39, which falls in line with all of the other devices and catheter-directed thrombolytic therapies which also seemed to result in a improvement into the RV LV ratio of very similar magnitude.
As far as the clinical outcomes, most patients stayed about one day in the ICU. 44 out of the 106 had zero ICU time. There was three days to discharge on average and we had one patient of all cause mortality, which turned out to be a patient that
died in hospice due to metastatic breast cancer. As far as major adverse events, we had no intracranial hemorrhage, no access site major bleeding, no decide related death, pulmonary injury or cardiac injury. We had one patient with a bleeding event and three patients with treatment
related clinical deterioration. The adverse bleeding event occurred very early in the clinical experience. This patient had hemoptysis and hemothorax after the procedure, and ended up being treated with a lobectomy.
We had three patients with clinical deterioration including worsening PE requiring surgery, cardiogenic shock requiring treatment for cardiogenic shock, and then one patient became agitated and VF-ed prior to actually having the procedure and was treated with defibrillation.
Of note, all four of these patients despite their major adverse clinical outcomes survived to the 30 day end point. I already talked about the relative improvement in RV to LV ratio. Relative to some of the other trails you've seen it falls directly in line and the safety,
I think the big safety note is that the major bleeding rate was quite low in this procedure with no major device related bleeding. So in conclusion, catheter-directed mechanical thrombectomy using the FlowTriever without the use of thrombolysis is safe and effective in improving RV function
in patients with intermediate risk PE. It's associated with a low ICU time, a low total hospital time, and I think it establishes a non-thrombolytic basis for acute, for treatment of acute pulmonary embolism. Certainly there's more investigation needed.
Thank you very much.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- Okay, it's great to be back. Thank you. So, moving on. So we know that inflammation is very important in the pathogenesis of cardiovascular disease. In this figure on the left, do you see how macrophages, mast cells, T-cells, all contribute to endothelial cell activation, eventually contributing to thrombus formation.
There is a large literature out there that when you measure biomarkers of inflammation in. In this figure on the right, when you measure levels of high sensitivity C-reactive protein, the higher the level whether you're on placebo, whether you're on aspirin, the higher your risk of cardiovascular events.
So, I think most people now believe strongly that you can discriminate cardiovascular risk by levels of inflammation in your blood. As low level, average, or high, depending on your level of high sensitivity CRP. Further to this, is this idea that when you look
at some of the statin therapy trials, like on the left, prove it, or even the ezetimibe trial on the right. When you lower both inflammation and LDL cholesterol, in the red bar, patients do better. If you don't lower LDL cholesterol or inflammation,
as seen in the blue bar, patients did really bad. If you lower one, regardless of which one it was, patients had this intermediate phenotype. So the lower your inflammation, the lower your cholesterol, patients do better. There is this idea that we have
this residual risk paradigm. Right? If you have an elevated cholesterol, as seen on the right side of this figure, then you have this residual cholesterol risk. Sorry, on the left side. If you have low cholesterol but you still have high levels of inflammation, you're believed to have
this residual inflammatory risk. So with this idea, the Cantos trial was performed. This was looking at canakinumab, which is an interleukin-1 beta receptor antagonist for the prevention of cardiovascular disease. Now, what's really interesting, is this figure on the left.
You see on the top, when you're looking at high sensitivity CRP, there was a dramatic reduction in CRP levels with this therapy. No difference in LDL cholesterol. No difference in HDL cholesterol, and no difference in triglycerides.
So finally we were going to be able to answer the inflammatory hypothesis. When you look at major adverse cardiac events, when you combine two of the doses of canakinumab, there was a significant 15% reduction in the incidence of cardiovascular events.
Now, the authors really nicely went back and saw, "What about the people who had "the greatest inflammatory reduction?" so those with the lowest levels of CRP, that's the red group right here. Showing that in that group that had
the lowest levels of inflammation, once again, had the lowest risk of cardiovascular events. So this was very exciting. But, there was some very significant adverse events. Adverse and actually pro. So in the green, you actually see that fatal cancer
was actually lower in the group that received canakinumab. But there was significant leukopenia, there was was significant thrombocytopenia in the group. So, this was sort of a mixed picture. I think because of this, and because of the less than compelling primary outcome,
the FDA as of a few weeks ago, did not approve this drug, for the reduction of cardiovascular events. So, I think it raises this hypothesis, but clearly it did not definitively stated, and we're not going to be giving it to patients
also because of this significant cost. So, what about other inflammatory drugs? As of three days ago, the New England Journal published this cert trial as an NIH funded trial. Looking at low dose methotrexate for the same purpose. Done by the same group of investigators.
As you can see, the hazard ratio was 0.96. There was no significant reduction in the endpoint of cardiovascular events. So, inflammation and cardiovascular disease. Is the inflammation hypothesis viable? I personally think the answer is yes,
but I believe that we need future trials that focus on specific pathways that will not have untoward side effects, that will be able to sort of target specifically what the issue is. I think future trials are being considered as we speak.
I think it's a very exciting time, but I think for once we can say that when you target inflammation, at least using the IL-1 receptor antagonist, you can lower the risk of cardiovascular events. Thank you very much.
- Alright, good morning, I'd like to thank Dr. Veith for having me here. Before I begin, I would just like to ask for a recount in the spirit of the times. So I'm going to try and bring us back on time and talk about the optimal medical therapy
for critical limb ischemia. These are my disclosures, non-relevant to this topic. So PAD patients, the mortality is high, as you all know. And in critical limb ischemia, the numbers are even worse as you can see here. The older the patients,
the more risk factors they have, the worse the mortality. And it is quite dismal over years. So treatment should definitely follow causes of mortality. So why do these patients die? So actually most of the reasons for these patients to die are actually nonvascular, as you can see here.
And it's obviously beyond the scope of this talk to explain what to do with these conditions, and obviously they're variable. But for cardiac and vascular causes of death, the treatment is medical and obviously not opening up the flow channel to be to the foot.
So just to answer the topic of the talk, my interim first conclusion is that even today, intervention is insufficient for CLI patients. And obviously medical therapy is key. But the goals of therapy should not only focus on the mortality,
but also obviously on morbidity. So my second interim conclusion is that for morbidity and complications, even in 2028, you know even in 10 years, medical therapy will not be sufficient to replace intervention.
And because I have very little time, instead of going into the data about each and every potential medical therapy that could be offered to these patients, I'd like to give sort of a focused bottom line and a few chosen medical therapies
that are relevant to this population. Anti-platelet therapies in peripheral artery disease, and obviously in CLI also, reduce mortality in a significant manner. And obviously patients with CLI should and will be, I think, still on an anti-platelet agent in the future.
Adverse events including mortality and vascular amputations are very much increased when patients have a major adverse limb event. And so for that reason, affecting these limb events is crucial. And identifying anti-platelet agents
that are safe but also reduce adverse limb events is key. So Vorapaxar did reduce acute limb ischemia. However, the price of excess bleeding, and for that reason is not being used routinely in these patients. However, I hope that in the future
we will have other options that targets not only mortality but also acute limb events. Ticagralor reduced both MACE and MALE, so both adverse cardiovascular events and also limb events. And so this is the cardiovascular events and this is the limb events.
And so it was very impressive in patients with PAD. What about a completely different mechanism? So plaque rupture may induce atherothrombosis, so there could be atherosclerosis as a result of plaque rupture with a thrombotic component, locally resulting in critical limb ischemia.
And indeed in this pathological study of 75 patients with CLI, post-amputation thrombosis in the lumen was seen in many of these patients. So is there a role for anticoagulation? Well you've heard of the COMPASS trial
in the previous session from two speakers, and indeed low-dose Rivaroxaban resulted in fewer events. And although there were more bleeds, there was net benefit for this therapy, which was recently approved by the FDA. Statins, as you've heard from most previous speakers,
reduce major adverse cardiovascular events, but also reduce adverse limb outcomes, specifically high-intensity statins. And what about PCSK9 inhibitors? Well the reason I put them here and not at the sort of cardiovascular events
is just because their use is still very limited. But still they were very impressive, specifically in the PAD sub-analysis of Fourier. And what you can see here, that there's a very low number needed to treat in order to reduce adverse cardiovascular events
with these medications, even if many of them were on high-intensity statins. So my third interim conclusion is that in my opinion, by 2028 every CLI patient will be on an anti-platelet agent, on a statin and perhaps another anti-lipid medication. And likely on an anticoagulant of some sort.
However, in 2028 I still think that CLI will remain a team sport. Medical therapy and intervention I think will still go hand in hand, and I don't think one will replace the other. Thank you very much.
- Thank you very much, I appreciate the invitation to this great meeting. So I'm going to talk a little more broadly about beta blockade, then Dr. Mollis, and let's review again some of the randomized control trial data. So, just like the first slide with prior speaker, this really kind of turned me on to beta blockade.
It did show a benefit to Atenolol over placebo, fairly far out with regards to when its effect really was manifest, but it started to change practice, and then really, the decrease one trial was a game changer based on, it was high risk vascular surgical patients all had a positive stress test, moderate dose of Bisoprolol,
and they found a significant reduction in death and MI out to 30 days, but as many of you are aware, many of these are discredited. They didn't really look back at decrease one to see if that was fraudulent of fictitious, but many of their further trials have since been discredited.
So then, the POISE Trial came, and again, this was previously mentioned, and it does include vascular, non-vascular patients, but 8300 patients, Troprolol, pretty high dose right around the time of surgery versus placebo, and you can see that the non-fatal MI was significantly reduced, as well as a composite endpoint,
but stroke and bradycardia were significantly increased, and in fact, if you look at this out to one year, you can see that it was a 16% increase in all cause mortality, no difference in CV mortality, and then again, non-CV mortality was increased 22% and caused 54 excess deaths
compared to placebo, so that's real. Put it another way, 1,000 patients treated with a beta blocker would benefit from reducing 12 MIs and six revascularization, but increase harm significantly with 13 deaths and six strokes. Some of these trials, again, were otherwise mentioned,
and this is in vascular surgical patients, howbeit, not just AAA patients, but about 50 in each group, relatively small, and with 30 day assessment, it again was 50 to 100 milligrams Metoprolol the day before or on the day of surgery, mortality was not significantly different at the time of their discharge.
Another, slightly larger trial in patients with diabetes and beta blockade, 100 milligrams of Metoprolol, at least two hours prior to the OR, and they did two tests dosing to make sure the patients tolerated this out to day eight, and then they did a control for those who had bradycardia
or hypotension weren't included, so about 460 patients in this trial, and again, early 30 day outcome, not significantly different, and out to 700 days, again, the composite of death and cardiovascular morbidities. Last trial in terms of this review, same dosing regimine, basically, with Metoprolol here, about 250 patients
in each group, and again, no significant difference at six months, but significantly increased intraoperative hypotension requiring treatment in intraoperative bradycardia. So, putting these together with meta-analyses, looking at the effect of beta blockade
and perioperative death, actually a significant increase based on this meta-analysis, and particularly more striking was the 73% increase in overall nonfatal strokes with beta blockade. Again, the thing it did reduce was nonfatal MIs out to 30 days, even if you did
discount the decreased trials. A database review was presented by Dr. Mallis, and this was a VA cohort study, slightly different one, 37,000 patients in the VA system propensity matched and had received beta blockade within one day of surgery and thereafter, and I'm pointing out that
the vascular surgical patients, whether they were low risk or high risk, all achieved no benefit from this. So again, it may be just as much an issue of two large a dose as too short of time for it to, the medication to be administered,
and if you don't totally disbelieve the decrease one trial, they found that when the heart rate was titrated less than 65 compared to over 65, the benefit was really striking there. So, what do the guidelines say about this? Well, the AHA and 2014 perioperative beta blockade
started with one day or less before non-cardiac surgery prevents non-fatal MI, but increases the risk of stroke, death, hypotension, and bradycardia. So, what do I recommend? Well, I think that you need to keep your patients on beta blockers, if they're on them for
any indication already, such as heart failure. If they're at high risk for perioperative MI, such as those with positive stress tests that aren't a candidate for revascularization, start low dose Metoprolol, and/or Atenolol, and at least 15 to 30 days in advance,
try to titrate that heart rate, avoid the dose on the morning of surgery, and really do need a randomized control trial of titrated low dose beta blockade in high risk patients, thank you.
- Thank you to the moderators, thank you to Dr. Veith for having me. Let's go! So my topic is to kind of introduce the ATTRACT trial, and to talk a little bit about how it affected, at least my practice, when it comes to patients with acute DVT.
I'm on the scientific advisory board for a company that makes IVC filters, and I also advise to BTG, so you guys can ask me about it later if you want. So let's talk about a case. A 50-year-old man presents
from an outside hospital to our center with left lower extremity swelling. And this is what somebody looks like upon presentation. And pulses, motor function, and sensation are actually normal at this point.
And he says to us, "Well, symptoms started "three days ago. "They're about the same since they started," despite being on anticoagulation. And he said, "Listen guys, in the other hospital, "they wouldn't do anything.
"And I want a procedure because I want the clot "out of me." so he's found to have this common femoral vein DVT. And the question is should endovascular clot removal be performed for this patient?
Well the ATTRACT trial set off to try and prevent a complication you obviously all know about, called the post-thrombotic syndrome, which is a spectrum from sort of mild discomfort and a little bit of dyspigmentation and up
to venous ulcerations and quite a lot of morbidity. And in ATTRACT, patients with proximal DVT were randomized to anticoagulation alone or in combination with pharma mechanical catheter-directed thrombolysis.
And the reason I put proximal in quotes is because it wasn't only common sort of femoral vein clots, but also femoral vein clots including the distal femoral vein were included eventually. And so patients with clots were recruited,
and as I said, they were randomized to those two treatments. And what this here shows you is the division into the two groups. Now I know this is a little small, but I'll try and kind of highlight a few things
that are relevant to this talk. So if you just read the abstract of the ATTRACT trial published last year in the New England Journal of Medicine, it'll seem to you that the study was a negative study.
The conclusion and the abstract is basically that post-thrombotic syndrome was not prevented by performing these procedures. Definitely post-thrombotic syndrome is still frequent despite treatment. But there was a signal for less severe
post-thrombotic syndrome and for more bleeding. And I was hoping to bring you all, there's an upcoming publication in circulation, hopefully it'll be online, I guess, over the weekend or early next week, talking specifically about patients
with proximal DVT. But you know, I'm speaking now without those slides. So what I can basically show you here, that at 24 months, unfortunately, there was no, well not unfortunately,
but the fact is, it did cross the significance and it was not significant from that standpoint. And what you can see here, is sort of a continuous metric of post-thrombotic syndrome. And here there was a little bit of an advantage
towards reduction of severe post-thrombotic syndrome with the procedure. What it also shows you here in this rectangle, is that were more bleeds, obviously, in the patients who received the more aggressive therapy.
One thing that people don't always talk about is that we treat our patients for two reasons, right? We want to prevent post-thrombotic syndrome but obviously, we want to help them acutely. And so what the study also showed,
was that acute symptoms resolved more quickly in patients who received the more aggressive therapy as opposed to those who did not. Again, at the price of more bleeding. So what happened to this patient? Well you know,
he presented on a Friday, obviously. So we kind of said, "Yeah, we probably are able "to try and do something for you, "but let's wait until Monday." And by Monday, his leg looked like this, with sort of a little bit of bedrest
and continued anticoagulation. So at the end of the day, no procedure was done for this particular patient. What are my take home messages, for whatever that's worth? Well I think intervention for DVT
has several acute indications. Restore arterial flow when phlegmasia is the problem, and reduce acute symptoms. I think intervention for common femoral and more proximal DVT likely does have long-term benefit, and again, just be
on the lookout for that circ paper that's coming out. Intervention for femoral DVT, so more distal DVT, in my opinion, is rarely indicated. And in the absence of phlegmasia, for me, thigh swelling is a good marker for a need
for a procedure, and I owe Dr. Bob Schainfeld that little tidbit. So thank you very much for listening.
- Thanks again for the invitation to talk about, I think a lot of excitement on these new medications, and you've heard a lot from our prior speakers. So, first focusing on antiplatelet, antithrombotic therapy, this very simple cartoon. Certainly, we've known about aspirin forever. Xa inhibitors, thrombin inhibitors,
the PAR inhibitors now are coming about to to prevent this atherothrombosis. And this, I think pretty well done analysis, looking at peripheral arterial disease patients, looked at which agents perhaps are the most efficacious. And what was shown here is ticagrelor and aspirin
or clopidogrel. Put another way that looks at both safety and efficacy, really, clopidogrel and ticagrelor and aspirin stand out more than aspirin alone. So you've already heard about the COMPASS Trial in a fair bit of detail, but again,
this was rivaroxaban plus aspirin versus aspirin alone. And this substudy in patients with a PAD specifically looked at MALE, AMP, et cetera. 6300 patients, and you can see a significant reduction with, again, rivaroxaban plus aspirin versus aspirin alone. 43% reduction MALE, 67% reduction to amputation,
decreased vascular interventions, but at the cost of increased bleeding. Vorapaxar is a PAR inhibitor. It's gotten a little less use because of the bleeding events, but of interest in patients, a substudy of patients with PAD, 3700 patients,
again, there was no difference in the composite CV outcome, but acute limb ischemia was significantly reduced, incident acute limb ischemia, and the need for revascularization. So there's a lot of these agents, and Dr. Hiatt, I think in this nice review in JAMA Insights,
helped clarify this with this table. So if you have asymptomatic patients with PAD, probably antithrombotic therapy aspirin may not be of benefit, but for patients with PAD-associated limb symptoms, probably clopidogrel or ticagrelor monotherapy
is most efficacious to prevent long-term cardiovascular events. Still, with patients with revascularization, a bypass aspirin should be maintained. For patients with polyvascular disease, PAD plus manifest CAD, again,
antithrombotic therapy for stable cardiovascular disease, either adapt or clopidogrel alone. For patients who are at risk of cardiac and ischemic limb events, either ticagrelor plus aspirin is probably better than Plavix, or low-dose rivaroxaban.
Again, you heard about the COMPASS Trial. And probably vorapaxar, less likely to recommend that. From Dr. Rockman, you just heard a nice overview in terms of LDL, but again, the greater the reduction, the greater the decrease in events. This meta-regression just shows
that it does matter where you start. So if you start at a pretty high LDL level, and you get one of these agents, you have a greater relative risk reduction as comparative if you're already starting fairly low. Again, from this same summary,
for patients that were already at a low level LDL, you still gained a benefit from the addition of the PCSK9 inhibitors without any increase adverse events. So, just again, you heard about this from the last speaker, but this, again, focusing on patients with PAD. Here, overall it was 27,000 patients in this large trial,
follow up, 2.2 years, and again, as was highlighted previously, those with PAD gained a greater benefit than those without PAD. And again, major adverse limb events significantly reduced, 37% over time.
How about ezetimibe that blocks cholesterol at the GI tract level. Safe drug, this was a randomized controlled trial of ezetimibe versus simvastatin, plus simvastatin. 18,000 patients, these weren't PAD-specific. Acute coronary syndrome was the inclusion.
And here, they really decrease the LDL from 70 to 54, with about a 7% decrease overall cardiovascular morbidity and mortality. Raising HDL, you heard from one of the very early speakers, this is off the market now, really not worthwhile to do. And Dr. Berger noted that this agent just was presented
the American Heart Association, I think it's very interesting, patients with hypertriglyceridemia in this derivative of Omega 3, iscosapent ethyl, five year out follow-up, and everything they looked at was significantly reduced,
which I think is quite exciting. So what should we do about our high-risk PAD patients? Aspirin, but really probably lean more toward Plavix should be the first line therapy for symptomatic PAD patients. Consider rivaroxaban in those with coronary artery disease
would be my first line, and again, reducing both cholesterol and inflammation with statins should be standard. If you can't get that LDL less than around 70, maybe add ezetimibe, that seems to be safe and efficacious. PCSK9 inhibitors in refractory patients,
particularly those that are still above 200, there seems to be no lower limit of LDL, and again, keep your eye on this new triglyceride-lowering drug. Thank you!
- So I don't have to give you any data. I just have to tell you how we do it. So this is the easiest talk of this session. Step-by-step technical tips. Now our definition of pharmaco-mechanical may vary between us so I'll give that as we go along. These are my conflicts.
When to use it. Well certainly as you already heard, Massive PE has contraindication to full dose lytic is one area. Submassive elevated risk may be another. We've already seen multiple people put up
these guidelines so what we're really talking about at this point in time is those patients that we just talked, that those two groups that they just talked about because those are the ones that we're trying to treat. The biggest thing is don't be frozen by indecision.
Majority of patients eligible for thrombolysis do not receive it. It's amazing to me as a referral center to get the call from an outside community hospital or the patient with hypotension, abnormal RV or biomarkers and they've barely given the patient
Heparin and they just want to transfer the patient out of there and you tell them that's a massive PE. Please give them systemic thrombolysis and they go what? And I go you now have 10 times the death rate of an acute myocardial infarction. Would you give this patient lytics for acute MI?
Yes. Then give them the freaking lytics. Save their life. It's amazing what's going on in this country. So the PERT Consortium and everything, we really need to educate the community
because it's ridiculous. If you look at the utilization of thrombolysis, it's going down. Unbelievable and if you look at the in-hospital mortality for these patients that have significant PE, the in-hospital mortality is much higher
if you don't give thrombolysis. You've already seen this indirectly in a bunch of different lectures, but I just wanted to show you very quickly how to do this on an echo or CT. You want to get the center line, get it at the valve and then measure it one centimeter
below that valvular plane. This is something you don't have to depend on radiology just to do. You can just look at the transfer CT. You can look at the echo. You don't have to fight with your echo guy to give you that.
It's also very evident and often times just looking at the images. Why treat submassive elevated risk PE? You know what? I've heard all the mortality stuff. I get it.
It doesn't change mortality that much. It does and we should measure it as a primary endpoint in our trials. Change your discharge time and in this day and age, medicine is so expensive. Time in the hospital, repeat procedures,
elevated your amount of treatment for that patient really has to be looked at as part of that, not just mortality. But there's eight times more recurrent PE and four times a mortality rate if you have a PE and unresolved RV dysfunction at discharge
and that should be looked at prior to discharge, not just say well they look like they're doing okay. Treatment of IVC, higher risk PE. Certainly the other thing we have to look at is there's other things to do. You've already heard a little bit
that there's IVC filters out there. We take out 90 some percent of our IVC filters in our section. We actually as a system now are up to 60% at seven months and it only takes effort. The patients that I see die in our hospital
in the last year that shouldn't have died are patients that should've gotten an IVC filter because they got heroic things to take out their PE and nobody put a filter in even though they had significant DVT left over because they were afraid of the TV commercials?
Oh my gosh. If you look at the 27 extra deaths that we've had from IVC filters that were removable in the United States, and you take our experience and multiply it by the number of tertiary care hospitals in the United States, use them when they're appropriate.
Take them out so the risk is low, but don't go away from them. They've already been shown to be beneficial for the right patient population. But you also have embolectomy and surgery should also be considered.
Step by step. Make the decision and clinically be consistent. PERT team or other consistent mechanisms. We have an app that we use. This is throughout our entire healthcare system so all the vascular specialists have this.
It's an algorithm that's supposed to be used both in the ER and for the different vascular specialties so everybody's being treated very similarly. We have all the different definitions. We have the PESI calculator. All this is in an app
that's readily available to our constituents. Special consideration certainly is the tolerance of thrombolysis, underlying tolerance of pulmonary hypertension. Again, we need to evaluate the patient, not just label them as a PE.
And I also think there's a special population we need to study and that's the socked in pulmonary artery with no perfusion on a CT scan. I think this is a different population long term and we need to study that a little bit more. We got to get the patient back from the edge.
I think I'm opposite of Jeff. I don't want to see them get worse and then treat 'em. I want to prevent them from getting worse as long as I'm selecting that population in a thoughtful matter. We primarily use low dose TNK.
This is nothing I'm going to give you data on. This is an institutional, what do you want to call it, anecdotal experience and we lost our contracts except for TNK so we had to go to this and so we do a lot of catheter-directed. You've already seen all these trials.
There's a ton of different devices out there. The one I want to talk to you about is using a really fancy one called a pigtail catheter and another one called an ethos catheter. This is a patient that had a significant PE. You can see that they've got bilateral main PE.
This is on table. This is what we do for the vast majority of our patients. We sit there, we use ultrasound guided access to the vein so that we cut down our venous complications for access site. The patient is given 20 and 30% of a loading dose
of TNK and then we watch them. If you look at thrombus in a test tube and you give a thrombolytic therapy, it takes about 20 minutes for fibrinolysis. So this is what we do. As you're going to see, this is over 25 minutes
and we see the patient went from a pulmonary pressure of 65 and a heart rate of 115 down to 25 minutes, the patient's pulmonary pressure is about 44 and their heart rate is in the 90's. This patient then has all the catheters removed on the table even though they got lytic
and they're heparinized. This is a venipuncture, so big IV. We send them up to the unit and we typically discharge them the next day. We have an echo B4 discharge to make sure there's been a significant recovery of RV.
If not we'll watch them an extra day and then all these patients get a CT again. I'm sorry an echo again at 30 days to make sure that we're getting good resolution from that. On table results, decrease your complications. Thrombolysis has always been associated with the
duration of thrombolytic therapy and intracranial bleed. Now you can either use a pigtail catheter which is what we use for most of these people because we can measure pressure in it. We spin it around a little bit in the pulmonary arteries and give the dosage.
Again, we give 20-30% of the dose. There is no data for that. If significant improvement does not occur, they'll get dripped overnight in the ICU at usually .5 to 1 milligram per hour. You've already seen the data for EKOS.
We use this if we think we need a little bit quicker Thrombolysis such as in a socked in pulmonary artery 'cause we have no flow. We do think that may help, but we don't have any data for that. It makes us feel good.
We spend a lot more money and so we think that may be reasonable at that point in time. This is just what it looks like when you put in bilateral EKOS catheters. Certainly the patient can be put in the ICU for this. I do think that we should do a trial looking at EKOS
with a little higher dose, do it for 30 minutes, look at those pulmonary pressures right on the table. I think, again, my own opinion is after 25 years, the closer we get to being done on table, catheters out, patients doing well, the better, safer procedure we have,
the less chance of mortality, the less chance of complication and as you decrease complications, your benefit improves. We've already seen the results and you'll see more of these from non-randomized trials such as Seattle 2 which looked at 150 patients,
but they saw very quick recovery of the RV which was very important. If you look at technical success, it was very high. The dosage of thrombolytic exceedingly lower, lower than what we're giving in a PTO catheter, that's for sure.
And if you look at the RV from Ultima Trial which was randomized. There was faster RV recovery utilizing this device. Thank you very much.
- Thank you Dr. Asher. What an honor it is to be up here with Dr. Veith and Dr. Asher towards the end. You guys are leading by example being at the end of the meetings. So, thank you for allowing me to be up and talking about something
that not a lot of vascular surgeons have experience with, including me. I have no disclosures. On your left, I have listed some of the types of diseases that we most commonly see in the vertebral artery, and there are quite a lot.
And on the right, the standard types of treatment that we pursue in vascular surgery or as a vascular specialist. And often, in the vertebral artery, if we are going to pursue treatment, it's the endovascular route.
But I'll talk a little bit about open surgery. The clinical presentation is often vague. And the things I wanted to point out here in this long list are things like alternating paresthesias, dysphagia, or perioral numbness may be something in the history to look for
that you may not be thinking about when you're thinking about vertebral basilar disease. The anatomy looks straightforward in this picture, with the four segments, as you can see. It gets a little more complicated with just the arterial system,
but then when you start looking at all these structures, that you have to get out of of the way to get to the vertebral artery, it actually can be a difficult operation, particularly even in the V1 segment. The V1 typically is atherosclerotic disease.
V2 is often compression, via osteophyte or musculo-tendon structures. And V3 and V4, at the top, are typically from a dissection injury from sort of stretch or trauma injury. The pathophysiology isn't that well understood.
You have varying anatomy. It's very difficult to access this artery. Symptoms can be difficult to read, and treatment outcomes are not as reliable. But I'm going to take you through a very quick path through history here in the description
of the V1 segment exposure by Dr. Rentschler from 1958. And I love these pictures. Here is a transverse incision over the sternocleidomastoid, just above the clavicular head on the right side. And once you get the sternoclavicular head divided, you can see the longus colli muscle there.
Anteromedial is the carotid. Of course, you surround that with a Penrose drain. And then once you do that, you can separate your longus colli, and deep to that, the vertebral artery just easily slips right up, so you can do your transposition.
It's not quite that easy. I've done one of these operations, and it was difficult finding t e. And, again, here is on the opposite side, you can see the transposition in this cartoon.
Dr. Berguer is the world's expert, and a lot of this open surgical work comes out of the University of Michigan. Here is a study looking at 369 consecutive extracranial vertebral artery reconstructions. You can see the demographics of clinical presentation.
And note that about 34% of patients are presenting with hemispheric symptoms, with 60% in the vertebral basilar distribution. 300 of these reconstructions were for atherosclerosis. And the outcomes were pretty good. Before 1991, there wasn't really a protocol in place
in assessing and doing these procedures. And you can see the stroke and death rates of 4.1 and 3.2% respectively. And then the outcomes after 1991 are considerably better with a five year patency rate of 80%. So, in summary, vertebral artery disease is,
I think if you review this, is somewhat under diagnosed. Revascularization is a viable option. Most often, it's endovascular. But if you have endo-hostility, then an open, particularly for the V1 segment, may be a better option.
And this requires people with good operative experience. Thank you very much.
- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years
of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).
It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,
it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases
that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it
was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.
And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted
inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted
selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.
In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients
stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.
This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,
and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,
and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.
- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,
valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction
but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique
to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the
sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness
but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have
smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.
Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse
and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap
we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid
valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility
to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put
in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction
disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.
- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper
that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.
Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.
So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.
The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.
And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome
certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups
and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written
and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?
If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.
If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk
of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.
We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,
quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,
but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.
So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.
It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.
And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.
- [Lecturer] Here we go. These are my disclosures. In 2013 the ACC and AHA wrote updated lipid management guidelines, which for the first time included specific recommendations for patients with peripheral arterial disease.
They also shifted the focus away from specific LDL targets, but instead they targeted statin intensity. This is the overview of the guidelines,
but in terms of the specific recommendations for PAD patients it's a fairly focused section. After excluding recommendations about dialysis patients because of a lack of data,
they basically broke it down that anyone with PAD who's less than 75 should be on a high intensity statin. Anyone above 75 should be on a moderate intensity statin.
What are the high intensity statins? These are the ones that you need to remember. It's Atorvastatin 40 or 80, or Rosuvastatin 20 or 40. This table is available in their paper
and in ours. We wanted to look at the impact of statins, and in particular the statin dosing. According to these guidelines, our patients undergoing revascularization
either endovascular or open surgery, for CLTI at our institution from 2005 through 2014 we used propensity scoring to account for baseline differences in patients. We had 11 hundred limbs
and 930 patients after excluding the dialysis cohort. Our follow up was 380 days. Our primary outcome was overall survival, but we also looked at major
adverse limb events, which has noted our amputation and major re-interventions. Our statin use over time did increase as of 2014. 90% of our patients
were discharged on a statin, but in terms of whether they were on the guideline appropriate dose, that was pretty dismal albeit the guidelines didn't come out until the end of this period.
When we looked at it based on age, you can see that in patients under 75, they're suppose to be on high intensity here in red and we're not very good at that although we were increasing over time.
Most were on moderate dose. In the patients over 75 who were suppose to be on moderate intensity we see that that's actually decreasing and largely being replaced
by high intensity statins. In terms of what's the benefit of statin versus no statin, there is a significant reduction in mortality and this is long term survival
in patients discharged on a statin compared to no statin. For limb events, there was a benefit in the sub group of patients over age 75 only.
When we looked to see if there was additional benefit to being on the guideline directed dose, we did find a significant benefit in overall survival
and in limb events in being on the appropriate intensity statin. Since there was a suggestion that in the older age group they should perhaps be on the moderate rather
than the high intensity statin, we looked specifically at this subject group and we actually did not find a significant difference between moderate or high intensity
dosing in that group. We also noted that adherence is poor so we wanted to look at what happened one year, how many patients stopped their statins or dropped the dose
and then how does that impact survival after a year. What we found is that it wasn't so much the guideline directed dose so much as just being on either a high
or a moderate intensity statin was associated with significantly improved survival compared to no statin or low dose statin after one year. We also found that 12%
of our patients stopped taking their statin or decreased the dose. The best survival was in those who remained on their statins and a close second was those who started statin
or increased their dose, but the patients who stopped taking their statin or dropped the dose had no survival benefit compared to patients who were never on a statin.
Statins are associated with an improved survival and a decreased limb events after revascularization for CLTI and the correct dose based on the 2013 ACC guidelines
does provide incremental benefit. 2/3 of our patients are not on the recommended doses. Moderate and high intensity statin after a year is associated with improved long term survival
and discontinuation or decreasing the dose is common and results in a loss of this benefit. It's not enough to just discharge patients on a statin,
we have to make sure that it's the right dose and we have to make sure that they stay on that during follow up. Thank you very much.
- Thank you for the opportunity to speak today. I have no disclosures. We've heard a lot about this, this morning, but, I'll just reiterate, for those of you who may or may not be familiar, The Fourier trial was a randomized trial of Evolocumab versus placebo in nearly 30,000 patients with atherosclerotic disease, and that the primary end point
was a composite of cardiovascular death, MI, stroke and hospital admission as well as some secondary end points as well. So what about these inhibitors in Peripheral Arterial Disease? Well, a sub analysis investigated the efficacy and safety of
Evolocumab in patients with PAD. And patients were defined as having PAD at baseline, if they had either intermittent claudication and an ankle brachial index of <0.85 or if they had a prior peripheral vascular procedure. So of the total cohort, 3,600 and some patients where 13%
had PAD based upon this definition, Evolocumab significantly reduced the primary end point consistently in patients with PAD with a hazard ratio of 0.79. What about Cardiovascular efficacy in the PAD population? Evolocumab significantly reduced both the primary end point
and the composite end point of cardiovascular death, MI or stroke very significantly and you can see in looking at this slides that the relative risk reduction was of higher magnitude in the patients with PAD than without PAD. Major advers limb events were significantly reduced in the overall population
as well as the patients with PAD and the results with regards to major amputation, I think are quiet compelling here. Again if you look at major advers limb event reduction you can see here in all patients and in patients with PAD there was a market reduction in events.
And then if we finally look at a composite outcome of MACE, and Male in patients with PAD, overall Evolocumab again reduced this composite outcome by nearly 21%, and if you look at the slide again, you can see that the magnitude of reduction, was of higher magnitude in the PAD group.
What about the safety? There were no differences in the incidents of adverse or serious events with the medication in patients with PAD. And importantly there was a consistent relationship between lower achieved LDL levels and lower risk of limb events that extended down to
very low levels of LDL cholesterol. So in summary Evolocumab significantly reduced the primary end point with patients with PAD because of their overall higher risk, patients with PAD actually had a larger absolute risk reduction for many of this end points than many patients without PAD and Evolocumab
significantly reduced major adverse limb events in all patients and in patients with PAD. What about Coronary disease as doctor Veith asked me to address? With in the of patients with prior MI, it was hypothesized that may be we could identify some that would
benefit more from this medication. So, 22,000 patients had a prior MI, and they were classified in several areas, one of them being, that based on the time of their most recent MI, 8,400 patients or 38 percent were with in two years of their most recent MI,
and this recent MI as well as other factors were independent predictors of a future cardiovascular outcome. So, if you see her in the placebo arm compared with patients with a remote MI , those with a recent MI were significantly higher risk in the placebo arm for the primary end point.
The relative risk reductions for the primary end point was greater in these high sub groups including recent MI, than for those with remote MI, and you can see this here in this slide as well. And patients with a recent MI and with remote MI and the magnitude of the reduction being much greater in the higher risk group.
So in conclusion recent MI, was felt to be a high risk condition and that these patients significantly benefit from cholesterol lowering with Evolocumab. So it's being reiterated here this morning, how low should we go, the targets are constantly changing and again changed just as recently as last week, and there
are a lot of good arguments for extensive lowering of LDL cholesterol, it's important to realize that because of the anticipated extreme reductions in LDL cholesterol regulatory agency require enhanced monitoring of adverse events. Particularly neuro-cognitive events, and in a sub study of FOURIER, there were no group differences in many of these
parameters between the placebo and medicated groups. in FOURIER the reduction in the primary and secondary composite end points was in fact linearly relate to the achieved LDL cholesterol. And in a post hoc analysis five percent of these patients achieved extraordinarely low levels.
In this group importantly, there were no associations between this achieved levels and predetermined safety event. So I tried very hard to find a slide that said when they go high we go low but unfortunately no one wanted to make that so I'll just say go low or go home.
- Thank you very much. So, this audience certainly knows that the higher the triglyceride, the greater the cardiovascular morbidity mortality, similarly if you have a low HDL that same relation holds, and certainly for the non-HDL-C or LDL-C calculated the higher the worse outcome and there's
multiple drugs related to this. Similarly with stroke, triglyceride the same relationship. Ischemic stroke increased with low HDL and again LDL-C correlates. So the historical precedent has been that you should get a fasting lipid level
when you first encounter the patient, but to make this simple that's really probably not true. So there's various things that are measured and that are calculated, but LDL is generally calculated, HDL is measured and then the triglycerides are calculated as remnant cholesterol.
So if you compare just the measured LDL compared to calculated LDL in a non-fasting state, it's a little bit of a wider linear relationship here as compared with the fasting, it's a little bit tighter. But when you look at this in more depth, and this reference here really nicely puts it all together
but the total cholesterol really doesn't vary if you've fasted one hour or 16 hours, similarly between men and women. The only thing that varies a little bit is triglycerides and we'll go on to that in just a little bit of depth.
But again that's variable, triglycerides go up if you eat really not much difference with the other lipid levels. And if you look just in terms of triglycerides, they overlap between non-fasting and fasting, really at almost all levels
so there's not really discrepancy. Similarly with LDL, same amount of overlap here whether or not you have diabetes it doesn't seem to make a difference. So for lipid panels, profile testing, in most patients you can get a non-fasting
initial lipid profile in any patient for cardiovascular risk assessment, I'd say that's where it's most commonly done in most of our practices. Similarly with acute coronary syndrome, if preferred by the patients et cetera.
But really it's where the non-fasting triglycerides are highly elevated that you want to get a fasting lipid panel. So what causes secondary hyperlipidemia related particularly to hypertriglyceridemia? Certainly certain diet factors, certain drugs,
cyclosporins for example, biliary obstruction and hypothyroidism. And so, one algorithm is that in terms of screening with non-fasting, and if it's less than 200 you're good to go, you really don't need to do anything further,
and if it's greater than 200 then probably a fasting lipid profile, lipoprotein panel is indicated. So reasons that non-fasting lipid measurement is fine most of the time is that again most trials have used non-fasting levels for determination of effectiveness of various medications.
This Friedewald formula actually uses total cholesterol, HDL, and triglycerides to calculate LDL-C, and LDL really is not directly measured, it's not standardized by the CDC such as these other cholesterol moieties are. And again most CV risk factor calculators don't use LDL-C.
So again, non-fasting is acceptable for the initial risk estimation in untreated and primary prevention screening. For patients with genetic hyperlipidemia probably fasting is required. Diagnosis of metabolic syndrome, non-fasting is fine.
And again some other more highly specialized scenarios you may want a fasting profile. Thank you.
- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations
related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,
and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be
a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation
of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest
as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher
patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.
The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence
that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization
versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,
in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,
one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients
who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored
superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months
for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.
But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear
to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.
Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so much.
- [Ron] (mumbling) Matt. - Okay, thanks Ron. So, I have some disclosures but they're not relevant to this talk. So, if we look at the EVAR-1 trial, a now very famous trial, we saw essentially, an early mortality advantage to EVAR. But then as you follow patients further out
there's a catch-up mortality. That's principally, being related to an increase in aneurism-related deaths, but because of the radiation involved some people have asked whether cancer rate can potentially play a role in the late catch-up of EVAR mortality.
So, from a theoretical basis, this is certainly possible. There's been a number of publications that have analyzed the amount of radiation that patients experience, both during the initial EVAR implantation and subsequently, in follow up. And certainly, from a theoretical basis,
you can see there might be an increase in cancer rates in EVAR patients. If you look further at the EVAR-1 trial, you actually do see that as you go further out in follow up, cancer rates in the EVAR group increase. So, if you look at all patients,
there's a 9% increase of cancer over the entire duration of follow up in patients undergoing EVAR. If you just look at patients out past eight years, there's nearly a doubling of the rate. So, I think these are the pertinent questions that
we need to ask about EVAR radiation and potential cancer. Is EVAR associated with an increased prevalence of cancer? Is this radiation related? Or is it related to the demographics of the patients, and what's implicated if there is an increase cancer rate? Is it the EVAR procedure itself, or is it the surveillance?
So, this was a study we performed a few years ago. It was an analysis using hospital episode statistics, so a national database in the UK. We looked at patients undergoing aneurism repair between 2005 and 2013, and we tracked new cancer diagnoses, hospital admissions, and cancer-related deaths.
So, in terms of the outcome measures, the primary outcome was survival free from abdominal malignancy or death. Secondary endpoints, we actually looked at freedom from lung cancer and non-abdominal obesity-related cancer, really just as control groups.
We also made an attempt to identify the centers that these patients were treated in for their EVAR, and whether these centers utilize duplex ultrasound follow up or CT scanning. So, just over 14,000 patients were analyzed who underwent EVAR.
Just under 25,000 undergoing open aortic surgery. If you look at the demographics, you can see that the patients undergoing EVAR are much older. They're sicker, and so results that I show you are going to be adjusted for age, deprivation index,
and medical comorbidities, as well as their location. So, these are the results. If you look at the freedom from abdominal malignancy or death, you can see that patients in the EVAR group have a 16% increase in their abdominal malignancy and death rate.
If you look at freedom from all cancers and death, you see a relatively similar result with a 10% increase in cancer and death from cancer in patients undergoing EVAR when compared to patients undergoing open surgery. What about the control groups?
Well, there's a significant increase, as I've said, in abdominal cancer and all cancer, but if you looked specifically at the control groups, that is patients who died or had a new diagnosis of either lung cancer or non-abdominal obesity cancer, you can see there's no significant increase there
in the EVAR groups, and that kind of suggests that it's the abdominal radiation that's causing these cancers. If you look at patients in the EVAR group who are undergoing either CT-based or duplex-based surveillance regimes, you can see there's no significant difference
between these two modalities. So, where does that leave us? Well, it leaves us with a finding that EVAR appears to be associated with an increase in abdominal cancer with no such association for either lung cancer
or non-abdominal obesity-related cancer. Doesn't appear to be a difference in abdominal cancer rates in patients undergoing EVAR that have been surveyed either with or without CT surveillance, or although, I think that's the least robust of the findings. What are the implications here?
Well, the implications are we clearly need to perform EVAR with as low a radiation dose as is reasonably achievable. And obviously, we've got a lot better with our dose reduction strategies. I think also, it does mean, given the CT exposure, that we need to challenge our surveillance paradigm,
given the fact that surveillance actually doesn't result in an improvement in aortic or all-cause mortality. Thanks very much for listening.
- 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.
- Thank you Michael for the invitation. We're going to look at this, these are m disclosures. And I wanted to focus on, so, we heard about Raghu presented the patient with this acute event big pulmonary embolism then we saw the imaging, we just saw which I think was very helpful and now we have to decide like,
what therapies are we going to use and we're not talking about thrombolytic therapy but what are the other alternative therapies and we're focusing really, mainly on this intermediate and this low-risk group since the massive PE group is going to have a more aggressive intervention for management.
So, if we look at these four trials that have been done out there, I just want to highlight for this audience the fact that, these patients were randomized to the standard treatment which was low molecular weight heparin then bridge to warfarin
and they were compared head-to-head. In Amplify and Einstein, the patients received the Rivaroxaban and Apixaban initially for the treatment of pulmonary embolism. So, it didn't have any kind of lead in therapy. I just want to show you that they excluded people
who actually got low molecular weight heparin or unfractionated heparin. So, they really had a good head-to-head comparison to the standard of care we know. The other two trials of course, had lead in therapy for their management.
That being said, everyone in the audience wants to know how bad were the PEs in these trials so, I put the two trials there, the Amplify study and the Einstein PE study showing that the patients did have substantial pulmonary embolism thrombus load in this patient population.
They were treating people that were involved extensively with pulmonary, not massive PE. So, it's good head-to-head comparison sort of challenging the standard of care that we know. Rachel and I wrote this paper to really look at, remember dosing correctly for this patient population
for in the trials, it's clear to remember that it's 21 days for Rivaroxaban at 15 milligrams twice a day and it's Apixaban is 10 milligrams twice a day. Often forgot because people start the patient immediately on the lower doses of these medication.
I highlighted all the trials together in one slide so you can see when you actually compare them to the standard of care, there's non-inferiority for each of the trials compared to low molecular weight heparin bridge to warfarin therapy in management.
So, I wanted you to see a composite of all the trials. The next thing all of us want to know, is what about bleeding and I put all the trials together and looking at the DOACs compared to the standard of care and many of you are looking at this and saying, "Gee, "it looks like the DOACs have a lower incidence
"of major bleeding compared to the standard of care," which was warfarin, remember now 'cause it's low molecular weight heparin bridge to warfarin. So, just keep that in mind that, when you look at this, the DOACs do have a lower incidence of major bleeding when you compare it to the standard of care
which is warfarin. They're not compared against each other but against the standard of care. So, if we have a PE, are we going to select a DOAC after that first initial assessment like we saw in Raghu's case, are we going to select a DOAC
at that point in time for management? Remember, what did Raghu select? They selected low molecular weight heparin bridge to warfarin standard of care? Could we have started that patient on a DOAC instead of the standard of care, because
according to the data I just show you, they're non-inferiority for the DOACs? We always like to go to a guideline. If you go to the ACCP Guideline 2016, I know there's a newer guideline coming out relatively soon, if a patient has no cancer, the recommendation
is to treat those patients for three months, that's the recommendation. If they have cancer, of course, they recommend low molecular weight heparin as part of that management over vitamin K antagonists or the DOACs.
And unprovoked PE which is another group that we're going to talk about here, the key here for us is to keep in mind is that, in that group, if there's a low risk for bleeding in the population, you want to do extended management with no date for stop. But if there's a high risk for bleeding,
you'll go with the lower time period of three months for the management and then follow those patients. Some new guidelines just came out on cancer, I just want to highlight them from, they're hot off the press 2018, both ISTH and NCCN, both now recommending that the DOACs and in this case,
they picked Rivaroxaban and Edoxaban based upon trials that these be part of the management now, considered part of the management of a patient who has malignancy and pulmonary embolism for their management. Some of you have not adopted that,
we have not gone whole hog on that at this point in time but I just wanted to highlight this for the group. Let's look at the unprovoked group. We saw in the case, Raghu looked at the patient for management, sent the gentleman out on low molecular weight heparin
and then switched that patient to warfarin therapy, bridged them over. We could have selected Apixaban or Rivaroxaban as the management for that gentleman but Raghu selected the standard management. Maybe he felt uncomfortable, I don't know.
But the data says, we could have used one of the DOACs. Now, you're out of the hospital and you're on a DOAC and you have to decide what you're going to do in terms of management. All of us are going to be treating the patients by standard management i.e. look at this this chart here
going through all the agents. And this is looking at preventing recurrence during that period of time in terms of management. This is preventing patients for longer term management looking at this group. Everyone, if you look at the trials here,
different dosing. Everyone gets treated with five milligrams of Apixaban twice a day, for three months and then if you're going to decide to extend management you can go to the lower dosing schedule of 2.5, twice a day and this was the comparison.
What can you glean from this? When you look at this, they looked at unprovoked VTE and what you can glean from this, if you look at the placebo groups here, look at the placebo group, patients who had placebo after being treated three or six months,
look the recurrence rate in the placebo group, 5.6, 8.8, 7.1 and of course, in the last study, there was no placebo group. What it shows us is the recurrence rate which all of us think about especially for the unprovoked PE.
Some of you in the room say, can you give us a risk index that can predict the patient who would get recurrent PE? I'm going to show you three risk tools that we would consider to use to define who would have recurrent events for PE.
I want to show you the Vienna Prediction Model which we use. You go online there to the, to the website, you do the calculation and it gives the patient something that you can discuss with them your risk of recurrence for an unprovoked PE
as your risk for recurrence of that event again. You can use the DASH Score, that's another score that's been used. Or you can use the MEN Continue and HER DOO2 Score, which I thought was very interesting, look at the parameters for this.
People have tried to give us, clinicians, a risk index to predict recurrence for unprovoked PE. Going back to this, I just want you to keep this in mind, the duration and look at the Riva study at the bottom where Aspirin was used. Some of us in the room,
I don't know how Jeff Olin feels about this or Rachel Rosovsky. You treated a patient for three months unprovoked VTE, the patient doesn't want to be on one of the agents, can aspirin be used as a prevention for recurrence? We all know there's two big Aspirin studies,
well, this is another addition to that Aspirin data looking at that as a prevention for recurrence. How do I look at this? I look at it as the first few days of the PE, the first day, one or two, remember, we want to get the patient out of the hospital
as quickly as possible 'cause Dr. Jeff will be very upset at your length of stay with respect to the management of PE. So, he's going to want to know, can you get them out quickly. I like to look at what's happening in that first day or so. Raghu did it in, I don't know, less than 24 hours,
he made the decision, got the patient out 'cause he wanted to leave. The point is, you need to decide what you're going to do in that first 24 hours, that's your decision point. In that decision point, will come up,
does the patient have resources for medication, where do they live, what's their family structure? And by the way, you're all doing that in light of the patient's pulmonary status with respect to how they are. Then you make that decision on what agent you're going to use,
pretty straightforward. Either you're going to use low molecular weight heparin during that phase of three to five days and then you're going to consider switching them over to the DOAC and then looking at the three to six month period where you select the DOAC for management
and finally, you'll decide if it's unprovoked or it's cancer or it's antiphospholipid antibody syndrome triple positive, you're going to decide then, one management is going to be for long term. So you can see, this truly is a team sport, it's not just the team getting together to discuss
if we're going to use catheter directed lytic therapy or not, it's really, that then plus all the management that comes with pulmonary embolism in the back end of the process. So, DOACs are here to stay, DOACs, I believe, can be used in the acute event
in that intermediate group. They've definitely shown to be non-inferior, lower risk of bleeding and I think they would be a successful long-term management in patients should you decide to do that. So, thank you very much.
- [Michael] A couple of questions on this Geno. First of all, not all acute PEs in the first, one to two days would you hospitalize on heparin-- - That's correct. That low-risk group. - [Michael] So, incidentally found
peripheral pulmonary embolus that the scan probably shouldn't have been done in the first place. You might even consider not treating those, I presume. - No, I would consider treating depending upon the circumstances Mike. If they're a cancer-based as part of staging,
I would treat those patients. It's that other group that's non-cancer incidental sub-segmental PE, I would not treat that. - [Michael] What data, just in general, changed those guidelines to include DOACs as a primary therapy for cancer associated VTE?
- I think the two trials, the Edoxaban study that was done, looking at Edoxaban in this population and the SELECT-D study which was done looking at Rivaroxaban versus Dalteparin for the treatment. Dalteparin was also the comparator in the Edoxaban study. Those two trials clearly showed that these agents do work
except, we must keep in mind, there was an increased incidence in major bleeding in those studies. You have to measure that. - [Michael] And what about in patients who have failed anticoagulation in cancer-associated VTE?
They have a diagnosis of a cancer-associated VTE, they're being treated for their cancer, they get whatever you want to use, low molecular weight heparin full dose, they have another event, do we have any data on the optimal therapy
for those patients? - Answer Mike's question, so you have a recurrence on management. The CHEST Guidelines actually recommend, increasing the dose of low molecular weight heparin as your approach to managing this patient population.
The DOACs, I don't have anywhere to go with them 'cause there's no increasing the dose to see more efficacy at this point in time, so, in low molecular weight heparin, my choice, increasing the dose, 20%. - [Michael] And how about antiphospholipid syndrome, that's a different marker, right?
- Yes, antiphospholipid antibody syndrome either triple positive or one positive, those patients the recommendations are, not to use DOACs and to stay with low molecular weight heparin bridge to warfarin therapy, that's what I would do. - [Michael] Do you ever try and monitor any lab tests
in patients on DOACs? - I don't but I can tell you, we just completed a study called ADIOS in which we measured plasma levels of Apixaban. And we showed, discontinuing the drug then looking at it while the patients were on the agent
and then after discontinuing for surgery. I got to tell you, I think plasma levels may be a way of telling us the anticoagulation status of a patient, by the way, there was no correlation with the 10A levels, that was sort of surprising.
We had positive 10A levels but the plasma level was less than 30 nanograms per deciliter. So, we were actually picking up positivity of factor 10A levels but yet, there was not a significant plasma level of the drug. So, I think the 10A levels are little too sensitive
to tell us the anticoagulation. And hopefully, that study will be published fairly soon. - Great Geno, thanks. - Thanks.
- Thank you, Ulrich. Before I begin my presentation, I'd like to thank Dr. Veith so kindly, for this invitation. These are my disclosures and my friends. I think everyone knows that the Zenith stent graft has a safe and durable results update 14 years. And I think it's also known that the Zenith stent graft
had such good shrinkage, compared to the other stent grafts. However, when we ask Japanese physicians about the image of Zenith stent graft, we always think of the demo version. This is because we had the original Zenith in for a long time. It was associated with frequent limb occlusion due to
the kinking of Z stent. That's why the Spiral Z stent graft came out with the helical configuration. When you compare the inner lumen of the stent graft, it's smooth, it doesn't have kink. However, when we look at the evidence, we don't see much positive studies in literature.
The only study we found was done by Stephan Haulon. He did the study inviting 50 consecutive triple A patients treated with Zenith LP and Spiral Z stent graft. And he did two cases using a two iliac stent and in six months, all Spiral Z limb were patent. On the other hand, when you look at the iliac arteries
in Asians, you probably have the toughest anatomy to perform EVARs and TEVARs because of the small diameter, calcification, and tortuosity. So this is the critical question that we had. How will a Spiral Z stent graft perform in Japanese EIA landing cases, which are probably the toughest cases?
And this is what we did. We did a multi-institutional prospective observational study for Zenith Spiral Z stent graft, deployed in EIA. We enrolled patients from June 2017 to November 2017. We targeted 50 cases. This was not an industry-sponsored study.
So we asked for friends to participate, and in the end, we had 24 hospitals from all over Japan participate in this trial. And the board collected 65 patients, a total of 74 limbs, and these are the results. This slide shows patient demographics. Mean age of 77,
80 percent were male, and mean triple A diameter was 52. And all these qualities are similar to other's reporting in these kinds of trials. And these are the operative details. The reason for EIA landing was, 60 percent had Common Iliac Artery Aneurysm.
12 percent had Hypogastric Artery Aneurysm. And 24 percent had inadequate CIA, meaning short CIA or CIA with thrombosis. Outside IFU was observed in 24.6 percent of patients. And because we did fermoral cutdowns, mean operative time was long, around three hours.
One thing to note is that we Japanese have high instance of Type IV at the final angio, and in our study we had 43 percent of Type IV endoleaks at the final angio. Other things to notice is that, out of 74 limbs, 11 limbs had bare metal stents placed at the end of the procedure.
All patients finished a six month follow-up. And this is the result. Only one stenosis required PTA, so the six months limb potency was 98.6 percent. Excellent. And this is the six month result again. Again the primary patency was excellent with 98.6 percent. We had two major adverse events.
One was a renal artery stenosis that required PTRS and one was renal stenosis that required PTA. For the Type IV index we also have a final angio. They all disappeared without any clinical effect. Also, the buttock claudication was absorbed in 24 percent of patients at one month, but decreased
to 9.5 percent at six months. There was no aneurysm sac growth and there was no mortality during the study period. So, this is my take home message, ladies and gentlemen. At six months, Zenith Spiral Z stent graft deployed in EIA was associated with excellent primary patency
and low rate of buttock claudication. So we have most of the patients finish a 12 month follow-up and we are expecting excellent results. And we are hoping to present this later this year. - [Host] Thank you.
- This is what we're going to talk about today. It's a vascular approach to hypertension and AV fistula. This implant was first designed in the early 2000s and directed, actually, at COPD, but then redirected to hypertension. Disclosures. Hypertension, as we age, is largely a result
of the loss of compliance in our arteries. Approximately 85% of uncontrolled hypertension patients are those over 50 with predominantly mechanical hypertension. This is the implant and the procedure. It's simply an AV fistula created
in the external iliac artery with an endovascular procedure done under local. Takes about an hour to do, and it creates a very precise AV fistula that doesn't grow over time, about four millimeters, mediated by the implant.
This is a just sort of appetizer before we get into the data. This is a patient done recently and presented in June of 2018. Patient in Toulouse, France. The difference from renal denervation, of course,
is that it get an immediate effect on the table, a very large drop in blood pressure. And you can see ambulatory blood pressure is roughly 30 points lower systolic, 20 diastolic. And as we'll see that's backed up by long-term data. This is the main body of data that's been generated
to date, a randomized trial in Europe, has six and 12 month data now, and we'll review that. So the Prospective Trial, 83 patients, 44 treatment, 39 control. All of these patients had to be on maximal medical therapy. And the exclusion criteria
were generally cardiovascular morbidities. You can see the groups are very similar. And actually, these results are for the prior renal denervation group. So of note, patients who have had prior renal denervation also respond to this therapy quite well.
Here you can see a very significant drop in both office and ambulatory blood pressure at six months. Here's the broader study. Both six and 12 month data with the right panel being a consistent cohort, just the patients that were not lost to followup.
But you see very consistent results. Again, significant drops, 26 points and 20 points for systolic and diastolic respectively. And if we look at 24-hour ambulatory blood pressure changes at six and 12 months, not quite as much, but still very significant, 13 drop
in both systolic and diastolic. There was a crossover group after six months. Those randomized to no therapy can be crossed over to the therapy, and we see that those respond as well, much smaller group. The primary complication in this procedure
is not congestive heart failure or anything like that, it's iliac vein stenosis. We see this with our other work in arteriovenous fistulas for dialysis. As we know, stent therapy for iliac vein stenosis is very successful in non-thrombotic patients,
and so all of these patients were treated with an iliac vein stent and all resolved without incident or recurrence. Some of these patients in the European study were done from the left and it's always done from the right to avoid the May-Thurner physiology.
Two patients didn't respond. And now the therapy is going into a much larger trial, a 500-patient randomized trial. This is an adaptive study, double blind, sham-controlled, and of course multicenter. These patients have to have, as a primary endpoint,
of 24-hour ambulatory blood pressure and then secondary endpoint of office blood pressure. The inclusion criteria are very rigorous. These patients have to be on maximal drug therapy. They have to be on that same drug therapy and have the same blood pressures on multiple checks
over a three-month period before they're randomized and stay on that same drug therapy, if possible, for six months after randomization. The exclusions are similar to the European study. So in summary we look at this technique of using an AV fistula to reduce blood pressure.
With denervation we don't have a procedural endpoint on the table. Often it's a smaller and less consistent blood pressure effect. What we don't talk about is the fact that autonomic nerves do regenerate,
it's dependent on renal artery anatomy, and there's some risk of renal artery injury, albeit small. But with an AV fistula there's a very immediate and significant effect. It's scalable and reversible with covered stent. It's independent of the renal artery anatomy,
and it's effective in patients with prior renal denervation and durable. Thank you very much.
- Ladies and gentlemen, I thank Frank Veith and the organizing committee for the invitation. I have no disclosures for this presentation. Dialysis is the life line of patients with end-stage renal failure. Hemodialysis can be done by constructing an A-V fistula, utilizing a graft or through a central venous catheter.
Controversy as to the location of A-V fistula, size of adequate vein and priority of A-V fistula versus A-V graft exists among different societies. Our aims were to present our single center experience with A-V fistulas and grafts. Compare their patency rates,
compare different surgical sites, and come up with preferences to allow better and longer utilization. We collected all patients who underwent A-V fistula or A-V graft between the years 2008 through 2014. We included all patients who had preoperative
duplex scanning or those deemed to have good vessels on clinical examination. Arteries larger than two point five millimeter and veins larger than three millimeter were considered fit. Dialysis was performed three times per week. Follow up included check for a thrill,
distal pulse in the arter non-increased venous pressure or visible effective dialysis and no prolonged bleeding. Any change of one of the above would led to obtaining
fistulogram resulting in either endovascular or open repair of the fistula. We started with 503 patients, 32 of which were excluded due to primary failure within 24 hours. We considered this, of course, the surgeon's blame. So we left with 471 patients with a mean age of 58 years,
51 were older than 60, there was a male predominance of 63%, and over half were diabetics. The type of fistula was 41% brachio-cephalic fistula, 30% radio-cephalic fistula, 16% A-V Graft, and 13% brachio-basilic fistula.
Overall, we had 84% fistulas and 16% grafts. The time to first dialysis and maturation of fistula was approximately six weeks. First use of grafts was after two weeks. 11 patients with A-V fistula needed early intervention prior to or after the first dialysis session.
In sharp contrast, none of the A-V grafts needed early intervention. 68 patients were operated for their first ever fistula without duplex scanning due to clinically good vessels. Their patency was comparable to those who underwent a preoperative scanning.
Looking at complications, A-V grafts needed more reintervention than fistulas. All of them were late. Infection was more prominent in the graft group and pseudoaneurysms were more prominent in the A-V fistula group, some of them occluded
or invaded the skin and resulted in bleeding. Here's a central vein occlusion and you can see this lady is after a brachio-basilic A-V shunt. You can see the swollen arm, the collaterals. Here are multiple venous aneurysms. Here's an ulcer.
When we looked at primary patency of A-V fistulas versus graft, A-V fistulas fared better than grafts for as long as five years. When you looked at 50% patency in grafts, it was approximately 18 months, in Fistula, 13. Here's an assisted primary patency by endovascular technique
and when we looked at the secondary patency for the first 24, two years, months, there was no difference between A-V fistulas and A-V grafts, but there's a large difference afterwards. Comparing radio-cephalic fistula to brachio-cephalic fistula there was really no big difference in maturation.
The time was approximately six weeks. As for primary patency there is a trend towards better patency with brachio-cephalic fistula after six months, one year, and two years, but it didn't reach statistical significance. For patients with diabetes,
differences were statistically significant. Brachio-cephalic fistula showed a trend toward shorter maturation time, needed less reintervention, and had a longer patency rate. In conclusions then, ladies and gentlemen, A-V fistula require a longer maturation time
and have higher pseudoaneurysm formation rate, but better patency rates compared to A-V grafts. A-V grafts have a faster maturation time, but more late interventions are required and infection is more common. Finally, diabetic patients have a better result
with proximal A-V fistulas. Thank you for the opportunity to present our data.
- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans
can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.
But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.
What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?
Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for
all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',
and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.
He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.
So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.
It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,
and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after
you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,
and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.
That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.
How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.
But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.
In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,
the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors
such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants
to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study
because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.
So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist
on maximal protection and assume that all radiation is dangerous. Thank you very much.
- So these are my disclosures. And let's start first of all for the merit to have them, what are the potential benefits? So we'd like to get rid for permanent rigid metallic cage. We'd like to restore vasomotion, angulation, eliminate instant restenosis of metallic stents which is hard to treat.
We also have to keep the ability of late luminal enlargement, preserve the target for CABG and freedom from long-term polymer exposure, inflammation, and it is very appeal to patients and physicians not to have a permanent implant.
But with all these we have seen what is the desire. The desired is to have this absorbed treated artery looks like, very nice healing. Large lumen compared to metallic DES. Does it really happens? And the question was driven initially from data from Europe,
that look on large registries that the results of 30 days and six months with Bioresorbable Scaffolds was acceptable except for one thing, which definite, probable stent thrombosis. 1.5% and 2.1% in the coronary, it is not acceptable. This was also driven or repeated in a similar magnitude
in ABSORB II and ABSORB III which were randomized trials comparing Xience, which was the drug eluting with metallic stents to BVS or Absorb, which showed again over time higher thrombosis rate for both of those randomized trials and this was despite the patients were on DAPT.
As a matter of fact, the recommendations were extended for the Absorb now to three years, for the duration of the absorption time. So the question was whether these were two early studies without implying good technique. And then what is the good technique?
You doing pre-dilatation, you're doing post-dilatation, you're doing imaging. And that was actually implemented later on. So if we look at the latest data that was presented with the Absorb, which was ABSORB IV studies,
now the stent thrombosis are better. They're only 0.7% at one year compared to 0.3% with Xience. It still looks a little bit higher numerically, but these are within the range of what you can expect from drug eluting stent. The other thing that this study showed,
if you look on ABSORB III-like studies, your results are going to be relatively much better that what you have seen with ABSORB III. But nevertheless, this first generation stent, if you can look at the totality of the data was still higher events compared to metallic stent.
Now why did we prolong the DAPT from three years? Because we do know that the three years we still have PLLA that is still there and it could dismantle and cause scaffold thrombosis. Now Abbott pulled out the technology from the market for commercial reasons.
I think the main reason was the fear from thrombosis and patients and physician didn't want to use it. And the ESC guidance just changed their recommendations to Class IIIC, which means you should not use it unless you doing it in clinical trials. So this is really was hampering on the whole field.
And the question, can we resuscitate from this situation. First of all, we need to know how to improve it. We have to improve the technique, PSP, imaging, prolonged DAPT, and also we have to improve the technology with thinner struts, improved mechanical properties.
Are these coming along? Definitely yes. We have a array of second generation BRS with 80 micron, 99 micron, 100 micron compared to 228, 170, 150 in the first generation. So we are going to see secondary generation scaffolds
that perhaps will solve all those issues which we have seen with the thrombosis. And indeed, if it's not going to come from the U.S., probably not very soon, it's coming from China. And look at the number of programs right now. Five programs completed First In Man,
two of them in randomized clinical trials, two already completed registries. So the data from China which is randomized, will come and we'll see how that goes. This is a project that I've been working on, Magnesium just to show you,
that if you compare Magnesium to ABSORB you see no thrombosis on the porcine model shunt. And this is even better than metallic DES stent. So I think we can able to solve the thrombosis rate. If we do that, then I think we see those technology coming back again.
What about the periphery? There's was one study at ESPRIT, very small one, with actually promising result. And again, it's up to the companies to see if they're going to encroach to the SFA program. So my final thoughts are that the unmet need
for Bioresorbable scaffolds remain despite improvement of second generation DES. The first generation BRS are inferior to the best in class DES and should not suitable for routine use. We always will have to show randomized trials
that at least we have known inferiority of Bioresorbable technique to metallic DES and then with second generation BRS we have the hope to make scaffolds great again. Thank you very much.
- I will be talking about new KDOQI guidelines. I know many of you have heard about KDOQI guidelines being revised for the past maybe over a year or maybe two. Yes, it is being done, and it is going slow only because it's being done in a very different way. It's more than an update.
It's going to be more of an overhaul for the entire KDOQI guidelines. We in KDOQI have looked at access as a solitary problem like we talked about grafts, catheters, fistulas for access, but actually it sort of turns out
that access is part of a bigger problem. Fits into a big ESKD lifeline of a patient. Instated distal patients come in many varieties. It can affect any age, and they have a lot of other problems so once you have chronic renal failure, renal replacement mortality fits in
only when it becomes Stage IV or Stage V. And renal replacement mortality is not just access, it is PD access, it's hemo access, it is transplant. So these things, we need to see how they fit in in a given person. So the new KDOQI guidelines concentrates more
on individualizing care. For example, here the young Darien was an 11 year old with a prune belly syndrome. Now he has failed PD. Then there's another person here who is Lydia who is about 36 or 40 year old lady
with a insulin dependent diabetes. Already has bad vascular pedicle. Lost both legs. Needs access. Now both these patient though they need access, it's not the same.
It's different. For example, if you think of Darien, he was in PD but he has failed PD. We would love to get him transplanted. Unfortunately he's got terrible social situation so we can't get him transplanted.
So he needs hemo. Now if he needs hemo, we need to find an access that lasts for a long time because he's got many years ahead of him. On the other hand we have Lydia, who has got significant vascular disease.
With her obesity and existing infectious status, probably PD won't be a good option for her. So she needs hemo, and she's obviously not a transplant candidate. So how are we going to plan for hemo? So these are things which we are to more concentrate
and individualize when we look at patients, and the new guidelines concentrate more on these sort of aspects. Doing right access for right patient, right time, and for right reasons. And we go about planning this keeping the patient first
then a life plan ESKD lifeline for the patient, and what access we are looking at, and what are the needs of the patient? Now this is also different because it has been done more scientifically. We actually have a evidence review team.
We just poured over pretty much 1500 individual articles. Recent articles. And we have looked through about 4000 abstracts and other articles. And this data is correlated through a workgroup. There a lot of new chapters.
Chapter specific surgery like peri-operative, intra-operative, post-operative, cat issues, managing complication issues. And we started off with the coming up with the Scope of Work. The evidence review team took the Scope of Work
and tried to get all the articles and sift through the articles and came up and rated the evidence using a certain rating system which is very scientific. The workgroup then kind of evaluated the whole system, and then came up with what is clinically relevant.
It's one thing for statisticians to say how strong evidence this is, but it's another thing how it is looked upon by the clinicians. So then we kind of put this into a document. Document went through internal and external review process.
This is the process we have tried to do it. Dr. Lok has been the Chair of the group. Myself and Dr. Yevzlin are the Vice-Chairs. We have incredible workgroup which has done most of the work. And here are the workgroup members.
We comprised of nephrologist, transplant surgeons, vascular surgeons, Allied Health personnel, pediatric nephrologist so it's a multi interventional radiologist and interventional nephrologist. This is a multi disciplinary group which has gone through this process.
Timothy Wilt from Minnesota was the head of the Evidence Review Team, who has worked on the evidence building. And now for the editorial sections we have Dr. Huber, Lee, and Dr. Lok taking care of it. So where are we today?
We have pretty much gone through the first part of it. We are at the place where we are ready for the Internal Review and External Review. So many of you probably will get a chance to look through it when it comes for the External Review and would love
to have your comments on this document. Essentially, we are looking at access in the context of end stage renal disease, and that is new. And obviously we have gone through and done a very scientific review, a very scientific methodology to try
to evaluate the evidence and try to come up with guidelines. Thank you.
- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed
is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome
is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement
and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.
So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.
We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy
which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures
that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.
As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.
So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,
and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.
So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.
It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,
'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula
and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.
It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically
a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.
Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal
vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.
Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding
the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody
who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test
confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,
so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,
although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.
It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get
a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.
And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,
immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.
We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.
So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,
and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.
DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,
when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- So, I'm going to probably echo many of the themes that Gary just touched upon here. These are my disclosures. So, if we look at the CHEST guidelines on who should get pharmacomechanical techniques, it is very very very sobering, and I apologize if the previous speakers have shown this slide,
but essentially, what's right now being disseminated to the American College of CHEST Physicians is that nobody should get catheter-directed thrombolysis, the concept of pharmacomechanical technique should really only reserved as a last-ditch effort if nothing else works, if you happen to have somebody
with extraordinary expertise in your institution, it could not be more of a damning recommendation for what I'm about to talk to you about for the next eight or nine minutes or so. So, then the question is, what is the rationale? What are we talking about here?
And again, I'm going to say that Gary and I, I think are sort of kindred spirits in recognizing that we really do need to mature this concept of the catheter-based technique for pulmonary embolism. So, I'm going to put out a hypothetical question, what if there was a single session/single device therapy
for acute PE, Gary showed one, that could avoid high dose lytics, avoid an overnight infusion, acutely on the table lower the PA pressure, acutely improve the function of the right ventricle, rapidly remove, you know, by angiography,
thrombus and clot from the pulmonary artery, and it was extremely safe, what if we had that? Would that change practice? And I would respectfully say, yes it would. And then what if this concept has already been realized, and we're actually using this across the world
for STEMI, for stroke, for acute DVT, and so why not acute pulmonary embolism? What is limiting our ability to perform single session, rapid thrombus removal and
patient stabilization on the table? Gary showed this slide, there's this whole litany of different devices, and I would argue none of them is exactly perfect yet, but I'm going to try and sort of walk you through what has been developed in an attempt
to reach the concept of single session therapy. When we talk about pharmacomechanical thrombectomy or thrombo-aspiration, it really is just one line item on the menu of all the different things that we can offer patients that present with acutely symptomatic PE, but it is important to recognize
what the potential benefits of this technology are and, of course, what the limitations are. When we look at this in distinction to stroke or STEMI or certainly DVT, it's important to recognize that during a surgical pulmonary embolectomy case, the clot that's able to be extracted is quite impressive,
and this is a very very very sobering amount of material that is typically removed from the patient's right heart and their pulmonary circulation, so, in order to innovate and iterate a percutaneous technology based on existing concepts,
it really does demand significant disruption to achieve the goals, we have not tackled this yet in terms of our endovascular tool kit. So, what is the role? Well, it's potentially able to debulk in acute PE, in an intermediate risk patient which would
ideally eliminate the need for overnight lysis, as Gary alluded to, but what if it could actually replace surgical embolectomy in high risk patients? I think many of us have had the conversation where we, we sort of don't know that's there a
experienced, comfortable surgeon to do an embolectomy within the building or within immediate access to the patient that we see crashing in front of our eyes. I'm very very lucky here in New York that I've incredible cardiovascular surgeons that are able to perform this procedure very very safely 24/7,
but I know that's not the case across the country. So, one of our surgeons who actually came from the Brigham and Women's Hospital in Boston developed this concept, which was the sort of first bridge between surgical embolectomy and percutaneous therapy, which is a large bore aspiration catheter,
it's a 22 French cannula that was originally designed to be placed through a cutdown but can now be placed percutaneously, and I think many of us in the room are familiar with this technology, but essentially you advance this under fluoroscopy into the right heart,
place the patient on venous-venous bypass, and a trap, which is outside the patient, is demonstrated in the lower left portion of the screen here, is able to capture any thrombotic material and then restore the circulation via the contralateral femoral vein,
any blood that is aspirated. Very very scant data on this, here's the experience from Michael and Kenny up in Boston where they tried this technology in just a handful of cases, this was followed by John Moriarty's experience from UCLA, where he actually argued a little bit of caution
using this technology, largely related to its inability to safely and reliably deliver it to the pulmonary circulation. To that end, AngieDynamics is funding a prospective registry really looking at safety and efficacy at delivering this device to the pulmonary circulation
and its ability to treat acute pulmonary embolism as well as any right heart clot, but that data's not commercially available yet. This is just one case that we did recently of a clot in transit, which I would argue could not be treated with any other technology
and the patient was able to be discharged the same day, I personally think this is a wonderful application of this technology and is our default strategy right now for a very large clot in transit. The second entrance to the space is the Inari FlowTriever device, which is a 20 French cannula,
it does not require a perfusion team in vein-vein bypass, the concept is simple, a 20 French guide catheter is advanced into the pulmonary circulation and these trilobed disks, which function like a stentriever for stroke are deployed in the pulmonary circulation, retracted to allow the clot to be delivered to the guide cath,
and then using manual aspiration, the clot is retrieved from the patient. Just a few case reports in small series describing this, this one in JACC two years ago, showing quite robust ability to extract a clot, this company which is a relatively small company funded a
single-arm prospective trial enrolling 168 patients, and not only did they complete enrollment last year, but they actually received FDA approval, now there is no peer-reviewed literature on this, it has undergone public presentation, but we, we really don't know exactly which patients were treated,
and so we really can't dissect this, I think there is a learning curve to this technology, and it's not, certainly, ready for broad dissemination yet, we just don't know which patients are ideal for it currently. Another technology, the Penumbra CAT8 system,
a market reduction in the size, an 8 French catheter based technology, this is exact same technology that's used for thrombo-aspiration for acute ischemic stroke, currently just in a slightly different size, and then a number of cases demonstrating its efficacy at
alleviating the acute nonperfusion of an entire lobe, as Gary was referring to previously, and this is one of our cases from our own lab, where you see there's no perfusion of the right, middle and lower lobe, I'm not sure if I can get these movies to play here, oh here it goes,
and so using sort of a handmade separator, we were able to restore perfusion again to the right, middle and lower lobe here, so just one example where, I think there is a potential benefit of thrombo-aspiration in a completely occluded segment.
There has been a wealth of literature about this technology, mostly demonstrating safety and efficacy, the most recent one on the bottom right in CVIR demonstrates the ability to acutely reduce the PA pressures on the table with the use of this technology, and to that end,
Akhi Sista, our faculty here this morning, is the national principal investigator of a US multicenter prospective study looking at exactly that, to try and prove that this technology is safe and effective in the treatment of submassive pulmonary embolism, so more to come on that.
Lastly, the AngioJet System, probably the most reported and studied technology, this is a 6 French technology by default, a wealth of literature here showing safety and efficacy, however, due to adverse event reporting, this technology currently has black box label warnings
in the treatment of acute pulmonary embolism, so clearly this technology should not be used by the novice, and there are significant safety concerns largely related to bradyarrhythmias and hypotension, that being said, again, it is a quite experienced technology for this. So where do we currently stand?
I think we clearly see there are several attributes for thrombo-aspiration including just suction aspiration, a mechanical stent-triever technology, and the ability to not just insanguinate the patient but actually restore circulation and not make the patient anemic, here,
you can see where these technologies are going in terms of very very large bore and very small bore, I placed the question marked right in the center which is where I think this technology needs to converge in order to lead to the disruption for the broad adoption of a single session technology.
So, numerous devices exist, all the devices have been used clinically and have demonstrated the ability to be delivered in aspirary pulmonary embolus, at present, unfortunately there is no consensus regarding which device should be used for which patients and in which clinical presentations,
we need many prospective studies to demonstrate the safety and clinical benefit for our patients, we desperately do need a single session therapy, again, I completely agree with Gary on this, but there is a lot of work yet to do. Thank you for your attention.
- Thank you very much, I'm honored to be here. These are my disclosures. So first, just scope of the problem. One in four deaths worldwide is related to thrombosis. It's the leading cause of death throughout the world. And in the United States it's the third-leading cause of cardiovascular death,
accounting for $1.5 billion a year. More people die of a PE than breast cancer, car crashes, and AIDS combined. And you can see here from a study by John Heit that this problem is not going away. So how can we change these statistics?
Will looking for occult malignancy in patients who present with VTE, or testing for thrombophilia change these numbers? So I thought I'd start with a case. This is a 55-year-old avid tennis player, presented with sudden-onset shortness of breath.
And she had swelling in her right lower extremity. Her CT, as you can see here, showed bilateral stem emboli, and she clearly has an RV dilatation. Her vital signs, she's tachycardic, hypoxic, tachypneic. But fortunately her blood pressure is well-maintained.
Her troponin is minimally elevated, and her echo did show that she was demonstrating RV strain, and as Brian showed you, she has an elevated, her RV/LV ratio is clearly greater than one. So she was considered high-intermediate risk because of the strain, the troponin,
the tachycardia, the hypoxia, and the decision was to proceed with catheter-directed thrombectomy and lysis. There was no identifiable cause for her PE. So the question is, should she undergo extensive screening
for an occult malignancy? Well we know that about 5% to 10% of patients who present with an idiopathic VTE will be diagnosed with a cancer within the subsequent one to two years. We know that.
So should we? Well let's look at the data. This was a recent review and meta-analysis of 10 studies over 2,300 patients, most of them prospective, although there were three randomized controlled trials
looking at limited versus limited plus some kind of extension. Limited is like basic labs, chest x-ray, and then the extension one, one of them was limited plus an abdominal CT scan. This was based on a meta-analysis
that this author Carrier did, where they found that limited screening found about 50% of the cancers. But when an ab CT was performed, that increased it to about 67%. So that's what led to
this first randomized controlled trial, 845 patients, limited screening plus limited plus an ab CT. The second one was limited screening plus limited screening plus a CT scan of the chest, abdomen, and pelvis.
And the third randomized controlled trial was limited screening plus a PET scan. And you can see here, no difference in the number of cancers detected at baseline or at follow-up with adding an ab CT, at baseline or with follow-up
by adding a chest abdomen pelvis, or adding a PET scan. The only finding was that in the PET scan group, at two-year follow-up more cancers were identified in the limited screening group. Which means that the PET scan
found more cancers to begin with, but importantly, there was no difference in survival. So this meta-analysis did show that the cancer rate that they discovered was about 5% of these patients
that presented with idiopathic VTE. There was no significant difference in patients who got limited screening versus extensive screening. However, they did notice and remark on the fact that the cancer prevalence did increase linearly with age. So patients that were over 50
had a sevenfold increase in being discovered with cancer. And it was lowest in patients under 50 and in women who were on estrogen. So maybe we could define a population that would benefit from screening. And that's what the RIETE group did.
They found six factors that they looked at. Male, over the age of 70, if you were a tobacco smoker, high platelet count greater than 350, anemic, or a past history of VTE. And they found that if you had two or less of these factors, 3.8% of patients were diagnosed with cancer.
But if you had three or more, that number went to 11.8%. So I think this scoring system actually may justify having a new study where you could evaluate extensive screening in a particular population of patients that you know have high-risk features. At this point, however,
the available data based on a number of guidelines do not support an extensive search looking for occult malignancy. However, very important to do a thorough history and physical exam, do some basic labs, and make sure that patients don't have signs or symptoms
suggestive of an occult malignancy. For example, they come in and they say, "Oh, I've had six months of dysphasia." That person probably warrants a work-up. Make sure they're up-to-date with age-appropriate cancer-related screening as well.
So going back to our patient, she had no signs or symptoms of malignancy, labs were normal, and she was up-to-date with her age-appropriate cancer screening. So now the question is,
should we test her for a hypercoagulable condition, either inherited or acquired risk factors? And what is the data for this? Well we know that patients who are diagnosed with VTE, about 50% of them actually will be identified with an inherited thrombophilia.
Factor V Leiden being the most, about 20%. Prothrombin G mutation about 8%. Antithrombin three deficiency, protein C, and protein S are much less. So that's a pretty big number, 50% of the patients. So should we do thrombophilia testing on everybody?
Well, will it change our management? Knowing this information, is it going to affect how long we keep people on blood thinners? Will it predict their recurrence? Will it help us guide in thromboprophylaxis?
Can identify family members? So maybe if that person has a daughter, they shouldn't be on estrogen. And will the testing cause any harm? Well at this point, routine testing is not warranted for everybody.
And in fact, if you have a provoked blood clot, there's no indication to do any of this testing. And these are published guidelines from many different organizations, including American Society of Hematology and Society for Vascular Medicine.
All say that thrombophilic testing really does not change or assist in clinical decision making. So as Dr. Jash mentioned earlier, do people follow this? Well this is a published paper out of Stanford just recently where they had a best practice alert.
So if you tried to order thrombophilia testing, this alert went up, and on the screen came up the Choose Wisely ASH guidelines. Which said, do not test for these people, consider testing for these people. And they saw who went along and then ordered the test.
So non-hematology specialists and general medicine providers, 50% of the time and 44% of the time respectively, followed those guidelines. Hematologists followed it 10% of the time. Unbelievable, right?
So, what about first unprovoked blood clot? Well we know those people, about 42% of them will have an inherited disorder. But remember, the inherited disorder did not cause the blood clot. The unprovoked nature of that blood clot,
that is what's going to predict their future recurrence risk, and that's what is going to dictate their length of anticoagulation. And we know this, Dr. Merle just mentioned this. The VIENNA Prediction Model. If you look at patients with unprovoked blood clots,
and you take them off their blood thinner, their risk of having a recurrent clot is up to 25% at five years, and some up to 50% at 10 years. And the other two he showed, the DASH and the HERDOO2, none of them have thrombophilia status in their model
to predict who's going to get recurrent clots. So what about testing to prevent primary prevention in family members? Well the guidelines vary. And studies actually do show that if you have a first-degree relative
that had a blood clot with an inherited risk factor, you have a higher chance of having that inherited risk factor and a higher chance of getting a VTE. But, family history alone, even without a positive thrombophilia testing,
increases your risk of getting a blood clot. So if you have one family member that's had a blood clot, you're twofold higher increased risk of getting a blood clot compared to the general population. If you have more than one family member, that's increased fourfold,
regardless of what your thrombophilia testing shows. So a negative thrombophilia screening does not equate to a normal VTE risk. Now whom should we test? There's a number of guidelines out there, I'll just mention three that were published
in the last one to two years, one in the New England Journal, one that just came out in Vascular Medicine. And they're good, it kind of walks you through. Does the person have a provoked blood clot, unprovoked, weak risk factor, consider this, consider that.
In general, what these guidelines are saying, is provoked, no screening. Unprovoked, you can consider it in these situations. So if you have a young patient with a really strong family history, and that patient may have a lot of female relatives
that are considering about getting pregnant or being on the pill, you can think about that. Patients with recurrent or extensive thrombosis, you want to think about antiphospholipid. Thrombosis in multiple sites, you want to think about myeloproliferative disorder.
Maybe APS, antiphospholipid, and also something called PNH, or paroxysmal nocturnal hemoglobinuria. That's pretty rare. If someone presents with Warfarin-induced skin necrosis you think about protein C deficiency.
Arterial thrombosis you think about the myeloproliferative and antiphospholipid. And patients with an unprovoked VTE and a low bleeding risk despite having a high one of those models, so you may have a high score of getting a recurrent clot, if they're thinking about going off anticoagulation,
would testing change your mind? I would test only in these situations and only if it's going to change your management of the patient or the family member. So what do I do? Provoked, no role.
And what I do is a very specific shared decision making model with the patient to go through, okay what happens if we get a positive test, and what are we going to do about that? Unprovoked in a strong family history in a young patient I think about it.
The unusual sites, think about the ones I just mentioned, antiphospholipid, PNH, or myeloproliferative. Arterial events, and recurrent events. So going back to our patient, she did great. But one month later,
and this was a patient before the DOAC, so she was on Coumadin. And she was really good about being adherent, and her INRs were always therapeutic. She reappeared with a new blood clot, and her ultrasound showed a new DVT.
So this is actually one situation that I do think about cancer, and in fact she had an abdominal CT scan which showed she had ovarian cancer. So in recurrent clots being on therapeutic anticoagulation, I do worry about cancer and I do think about it.
So my closing reflections. Extensive screening for cancer in idiopathic blood clots is not indicated. However, please make sure that you are doing a thorough history, physical exam, basic labs, following up on any abnormal testing,
and making sure patients are appropriate age, appropriate cancer-related screening. Thrombophilia testing, it's not indicated in most situations. Definitely not in a provoked blood clot. But you can think about doing it in an unprovoked blood clot
if it is going to change your management of that patient or the family member. And remember to think about the risks and benefits and really be thoughtful about it. Thank you very much.
Thanks very much, Tom. I'll be talking about thermal ablation on anticoagula is it safe and effective? I have no disclosures. As we know, extensive review of both RF and laser
ablation procedures have demonstrated excellent treatment effectiveness and durability in each modality, but there is less data regarding treatment effectiveness and durability for those procedures in patients who are also on systemic anticoagulation. As we know, there's multiple studies have been done
over the past 10 years, with which we're all most familiar showing a percent of the durable ablation, both modalities from 87% to 95% at two to five years. There's less data on those on the anticoagulation undergoing thermal ablation.
The largest study with any long-term follow up was by Sharifi in 2011, and that was 88 patients and follow-up at one year. Both RF and the EVLA had 100% durable ablation with minimal bleeding complications. The other studies were all smaller groups
or for very much shorter follow-up. In 2017, a very large study came out, looking at the EVLA and RF using 375 subjects undergoing with anticoagulation. But it was only a 30-day follow-up, but it did show a 30% durable ablation
at that short time interval. Our objective was to evaluate efficacy, durability, and safety of RF and EVLA, the GSV and the SSV to treat symptomatic reflux in patients on therapeutic anticoagulation, and this group is with warfarin.
The data was collected from NYU, single-center. Patients who had undergone RF or laser ablation between 2011 and 2013. Ninety-two vessels of patients on warfarin at the time of endothermal ablation were selected for study. That's the largest to date with some long-term follow-up.
And this group was compared to a matched group of 124 control patients. Devices used were the ClosureFast catheter and the NeverTouch kits by Angiodynamics. Technical details, standard IFU for the catheters. Tumescent anesthetic.
And fiber tips were kept about 2.5 centimeters from the SFJ or the SPJ. Vein occlusion was defined as the absence of blood flow by duplex scan along the length of the treated vein. You're all familiar with the devices, so the methods included follow-up, duplex ultrasound
at one week post-procedure, and then six months, and then also at a year. And then annually. Outcomes were analyzed with Kaplan-Meier plots and log rank tests. The results of the anticoagulation patients, 92,
control, 124, the mean follow-up was 470 days. And you can see that the demographics were rather similar between the two groups. There was some more coronary disease and hypertension in the anticoagulated groups, and that's really not much of a surprise
and some more male patients. Vessels treated, primarily GSV. A smaller amount of SSV in both the anticoagulated and the control groups. Indications for anticoagulation.
About half of the patients were in atrial fibrillation. Another 30% had a remote DVT in the contralateral limb. About 8% had mechanical valves, and 11% were for other reasons. And the results. The persistent vein ablation at 12 months,
the anticoagulation patients was 97%, and the controls was 99%. Persistent vein ablation by treated vessel, on anticoagulation. Didn't matter if it was GSV or SSV. Both had persistent ablation,
and by treatment modality, also did not matter whether it was laser or RF. Both equivalent. If there was antiplatelet therapy in addition to the anticoagulation, again if you added aspirin or Clopidogrel,
also no change. And that was at 12 months. We looked then at persistent vein ablation out at 18 months. It was still at 95% for the controls, and 91% for the anticoagulated patients. Still not statistically significantly different.
At 24 months, 89% in both groups. Although the numbers were smaller at 36 months, there was actually still no statistically significant difference. Interestingly, the anticoagulated group actually had a better persistent closure rate
than the control group. That may just be because the patients that come back at 36 months who didn't have anticoagulation may have been skewed. The ones we actually saw were ones that had a problem. It gets harder to have patients
come back at three months who haven't had an uneventful venous ablation procedure. Complication, no significant hematomas. Three patients had DVTs within 30 days. One anticoagulation patient had a popliteal DVT, and one control patient.
And one control patient had a calf vein DVT. Two EHITs. One GSV treated with laser on anticoagulation noted at six days, and one not on anticoagulation at seven days. Endovenous RF and EVLA can be safely performed
in patients undergoing long-term warfarin therapy. Our experience has demonstrated a similar short- and mid-term durability for RF ablation and laser, and platelet therapy does not appear to impact the closer rates,
which is consistent with the prior studies. And the frequency of vein recanalization following venous ablation procedures while on ACs is not worse compared to controls, and to the expected incidence as described in the literature.
This is the largest study to date with follow-up beyond 30 days with thermal ablation procedures on anticoagulation patients. We continue to look at these patients for even longer term durability. Thanks very much for your attention.
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