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The PREPIC Trial: Fact Or Fiction
The PREPIC Trial: Fact Or Fiction
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What's Next | AVIR CLI Panel
What's Next | AVIR CLI Panel
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Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
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Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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Claudication vs CLI | CLI: Cause and Diagnosis
Claudication vs CLI | CLI: Cause and Diagnosis
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The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
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CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
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PAD and Diabetes | CLI: Cause and Diagnosis
PAD and Diabetes | CLI: Cause and Diagnosis
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Case Example | Management of Patients with Acute & Chronic PE
Case Example | Management of Patients with Acute & Chronic PE
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General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
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Why Treat Carotid Occlusive Disease? | Carotid Interventions: CAE, CAS, & TCAR
Why Treat Carotid Occlusive Disease? | Carotid Interventions: CAE, CAS, & TCAR
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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Overview of PAD & CLI | CLI: Cause and Diagnosis
Overview of PAD & CLI | CLI: Cause and Diagnosis
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PE Management | Management of Patients with Acute & Chronic PE
PE Management | Management of Patients with Acute & Chronic PE
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PE Overview | Management of Patients with Acute & Chronic PE
PE Overview | Management of Patients with Acute & Chronic PE
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Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
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Outcome data | Uterine Artery Embolization The Good, The Bad, The Ugly
Outcome data | Uterine Artery Embolization The Good, The Bad, The Ugly
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
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Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
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PE Case Intro | Management of Patients with Acute & Chronic PE
PE Case Intro | Management of Patients with Acute & Chronic PE
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CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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PAD/CLI Diagnosis | CLI: Cause and Diagnosis
PAD/CLI Diagnosis | CLI: Cause and Diagnosis
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Definitions in PE | Pulmonary Emoblism Interactive Lecture
Definitions in PE | Pulmonary Emoblism Interactive Lecture
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Ideal Uterine Fibroid Embolization Candidates | Uterine Artery Embolization The Good, The Bad, The Ugly
Ideal Uterine Fibroid Embolization Candidates | Uterine Artery Embolization The Good, The Bad, The Ugly
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Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
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Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
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Malignant Biliary Strictures | Biliary Intervention
Malignant Biliary Strictures | Biliary Intervention
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Transcript

- Afternoon. It's a privilege to be presenting this today. I have no disclosures. If you look at this, this is a picture of the last 10 IVC filters approved by the FDA. You'll notice that they all have some mechanism of removal most commonly hooks.

You may ask yourself, why is that? And the reason for this is basically one or two studies. Basically the PREPIC study which was originally published in 1998 with two-year data, followed by a publication in Circulation with eight-year data.

Now the PREPIC itself, the study itself was the first prospective, randomized trial comparing anticoagulation to IVC filters. It was performed from 1991 to 1995 in France. 400 patients with DVT that were considered at risk for PE were enrolled.

And they were randomized at first either unfractionated versus fractionated heparins, and then IVC filter versus no IVC filter. And the filters used are demonstrated here, the Greenfield, the Cardinal, LGM, and Bird's Nest. And all patients were anticoagulated with warfarin

at the time of discharge whenever possible. Primary outcome was pulmonary embolism. The secondary outcomes were DVT, death, major filter complications, and major bleeding. And again, the data was published at two and eight years. So the two-year results, the PREPIC study,

they presented first some data on unfractionated versus fractionated heparin, but then this table. And this table shows basically that there was no difference in symptomatic PE between groups. But there was a difference in recurrent DVT

with patients having a filter in place having a higher incidence of DVT than those that did not. And the thought was that this presence of the filter increased the risk of DVT. Now the data at eight years, published in Circulation, did show a difference between symptomatic pulmonary embolism

with patients having a filter having a lower incidence of recurrent PE. However, the symptomatic DVT remained elevated in patients that had filters in place. And this was statistically significant. Of note, there was a fairly significant number of patients

that had cable thrombosis in the group that had filters that may have contributed to this number. So if you want to be critical about the study, there are a few things that are a little bit unperfect I guess you could say. It's now thought as a study of filter randomization

in patients with DVT, but it was actually also a study looking at unfractionated and low molecular weight heparins. And this lends itself to be a fairly weak study designed to make conclusions on IVC filters, the performance of IVC filters, and it's underpowered really to make a definitive conclusion.

The other problem with this study is that there's a wide variety of filters, I mean a Bird's Nest and the Greenfield, they're very different filters. And that lack of standardization I think is problematic. These filters both can have different rates

of IVC thrombosis, which can affect the data. So the statistical analysis was less than perfect. They should have corrected for multiple comparisons which they did not. And it also showed that PE can occur remotely, and if you don't have a filter in place,

it's probably not protective, obviously. So a PREPIC study was recently published, the PREPIC 2 in 2015. And this asks the question, do patients with acute PE at high risk of recurrence benefit from IVC filter in addition to anticoagulation?

So it was a multicenter trial in France. They had about 400 patients that were randomized, half into filters, half into no filters. Their risk factors are listed, and they're quite broad. And all filters were removed at three months. And they had follow up at three and six months.

And this is the data. The data at three months shows that there was no difference in recurrent PE between the patients with filters and the patient without filters. And at six months this remained the same. And there was no difference in DVT

between groups at six months. So fact or fiction? Well I think the PREPIC studies are mostly fact with maybe a little bit of fiction thrown in. The data from PREPIC suggests that patients with IVC filters have an increased risk of DVT long term,

but a decreased risk of PE long term. PREPIC 2 suggests that IVC filters may not decrease the risk of PE in high-risk patients, and did not show an association between filters and recurrent DVT at six and three months. Thank you.

after having these two cases one in our institution and one at University of North Carolina Chapel Hill that we would then basically upsize our particles to

100 micron and we have not seen that and we're doing a second clinical study and I'm not seeing that as either we had about a 70% reduction in pain so if you look at our visual analog score out to six months and if you look at our

disability it actually paralleled this exactly which is pretty impressive considering mostly patients had bilateral knee pain so out to six months very good results 90% of patients were responders so two

out of our twenty patients did not really respond one patient didn't respond at his one-month follow-up but did respond at his three and six so I still consider him a clinical failure because we expect

these patients to respond by one month here's just an example of a baseline MRI before and after and you can see all that joint effusion there the white that decreases just even after a month how much it decreases and we looked at this

in terms of synovial thickness and distension and even on MRI you can object objectively count calculate synovitis scores and we calculated that they actually statistically decreased this is another patient on the left the

image shows diffuse white enhancement if you will of the synovium of the lining on the right it shows the fluid this is an image just of embolization and I show this image because it's really shocking and this is actually one of our nurses

who's enrolled in a clinical study is this is before this is all we did we embolized the medial aspect of the knee this is one month later 30 days in fact somebody just asked me this when I was in the booth over at the meeting across

the street and basically I said listen I don't know why this happened so quickly I have no idea we didn't tap renu-it into anything else if you look at this premium post it's pretty dramatic so clearly there's an inflammatory process

that we are arresting or stopping in such a short period of time so is there a future for this I don't know it may just we may just fall down and find out that there really is in a great future but so far we know it's at least

technically successful it's the results are positive in the short term long term we're not so sure yet we do need to better understand these risks and I think in my opinion in the long term it'll probably be really really good for

this 40 to 65 year old patient population who's not yet ready for knee replacement surgery this is the algorithm for our clinical study which were almost done enrolling right now it's a randomized control study against

placebo so it's two to one randomization which means one third of the patients actually get a sham procedure so we do an angiogram on their leg they're asleep they have no idea for embolizing they're genetical it arteries or not we wake

them up I think about the table and we follow them up if they're no better they're allowed to cross over and get the treatment the other 2/3 of the

PE the first one of course is

anticoagulation so heparin and bridging the patient to coumadin or now aid a direct oral anticoagulant is really the mainstay of treatment most patients again 55 percent of patients with PE have low risk PE all of those patients

should be on according to the chest guidelines three months of anticoagulation so they're gonna get heparin as an inpatient if they even need it and they're gonna get sent home on lovenox bridge to coumadin or they're

gonna get the one of the new drugs like Xarelto or Eliquis but here's all the other things that we do so these patients that are in the intermediate high risk so I'm gonna try to keep saying those terms to try to kind of put

that in everyone's brain because I think the massive and sub massive PE is what everyone used to talk about but we want to keep up with our colleagues in cardiology who are using the correct terminology we're gonna say high risk

and an intermediate but in those patients - intermediate high risk or Matt or the high risk PE patients we're gonna be treating them with systemic thrombolysis catheter directed thrombolysis ultrasound assisted

thrombolysis and maybe some real lytic and elected me or thrombectomy there's other techniques that we can use for one-time removal of clot like rotational and electa me suction thrombus fragmentation and then of course

surgical mblaq t'me so when anticoagulation is not enough so I like to show this slide because it shows the difference between anticoagulation and thrombolysis they are very different and sometimes I think everybody in this room

understands the difference but I think our referring providers don't and so when we when we get consulted and we recommend anticoagulation they're like yeah TPA well that's not the right thing so anticoagulation stops the clotting

process so when you start a patient on a heparin drip they should theoretically no longer before new thrombus on that thrombus so when you have thrombus in a vessel you get a cannon you get a snowball effect more

and more thrombus is gonna want to form heparin stops that TPA however for thrombolysis actually reverses the clouding process so that tissue plasminogen activator or streptokinase or uro kindness will actually dissolve

clot so there you're stopping new clot forming versus actually dissolving clot anticoagulation allows for natural thrombolysis so your body has its own TPA and so when you put a patient on heparin you're allowing your natural

body defenses to work you're giving it more time TPA accelerates that process so you give TPA either systemically or through a catheter you're really speeding up that process anticoagulation on its own has a

lower bleeding risk you're putting a patient on heparin or Combe it in it's it is less but it is still real thrombolysis however is a very very high bleeding risk patients when I when I consult a patient for thrombolysis I

tell them that we are about to do give them the absolute strongest blood clot thinning agent or an reversal agent which is the TPA and we're gonna just run it through your veins for hours and hours

um and that sort of gives them an idea of what we're doing anticoagulation in and of itself is really not invasive you just give it through an IV or even a pill thrombolysis however is given definitely through an IV through

systemic means and a large volume there thereafter or catheter directed so again

now that you all have an overview and a refresher of nursing school and how these medications work in our body I want to now go over our practice

guidelines and the considerations that we take into place so as you know I'm not going to go over into detail the patient populations that are prescribed these meds but kind of knowing that these are the

patients that we see in our practice that for example are on your direct direct vector 10a inhibitors patients with afib or artificial valves or patients with a clock er sorry a factor v clotting disorder these oral direct

thrombin inhibitors patients with coronary artery thrombosis or patients who are at risk for hit in even patients with percutaneous coronary intervention or even for prophylaxis purposes your p2 y12 inhibitors or your platelet

inhibitors are your cabbage patients or your patients with coronary artery disease or if your patients have had a TI AR and mi continued your Cox inhibitors rheumatoid arthritis patients osteoarthritis vitamin K antagonists a

fib heart failure patients who have had heart failure mechanical valves placed pulmonary embolism or DVT patients and then your angiogenesis inhibitors kind of like Kerry said these are newer to our practice these are things that we

had just recently really kind of get caught up with these cancer agents because there really aren't any monitoring factors for these and there is not a lot of established literature out there knowing that granted caring I

did our literature review almost two years ago now so 18 months ago there is a lot more literature and obviously we learned things this morning so our guidelines are reviewed on a by yearly basis so we will be reviewing these too

so there is more literature out there for these thank goodness so now we want to kind of go into two hold or not to hold these medications so knowing that we have these guidelines and we'll be sharing you with you the tables that

tell us hold for five days for example hold for seven days some of these medications depending on why the patient is taking them are not safe to hold so some of the articles that we reviewed showed that for sure there's absolutely

an identified risk with holding aspirin for example a case study found that a patient was taking aspirin for coronary artery disease and had an MI that was associated with holding aspirin for a

radiology procedure they found that this happened in 2% of patients so 11 of 475 patients that sounds small number but in our practice we do about 400 procedures in a week so that would be 11 patients in one week that would have had possibly

an adverse reaction to holding their aspirin and then your Cox inhibitors or your NSAIDs as Carrie already mentioned it's just really important to know that some of those the Cox inhibitors have no platelet effects and then your NSAIDs

can be helped because their platelet function is normalized within 24 to 48 hours Worf Roman coumadin so depending on the procedure type and we'll go into that to here where we have low risk versus moderate to high risk

we do recommend occasionally holding warfarin however we need to verify why the patient is absolutely on their warfarin and if bridging is an option because as you learn bridging is not always on the most appropriate thing for

your patient so when patients on warfarin and they do not have any lab values available that's when you really need to step outside of guidelines and talk with your radiologists your procedure list and potentially have a

physician to physician discussion to determine what's best for a particular patient this just kind of goes into your adp inhibitors and plavix a few of the studies that we showed 50 are sorry 63 patients who took Plex within five days

of their putt biopsy they found that there was of those one bleeding complication during a lung biopsy so minimal so that's kind of why we have created our guidelines the way we did and here's just more information

regarding your direct thrombin inhibitors as cari alluded to products is something that we see very commonly in our practice and then your direct vector 10a inhibitors this is what we found in the literature

massive PE well let's remember this at this point including all the trials that preceded the pytho trial almost 1 700 patients have been randomized into systemic lytic trials for some massive p yep all we have on the CDT side is the

ultimate trial of 59 patients non-us single was a single trial that's where this initiative is coming from to improve the data this trial called P track and I have preliminary information that we just made our first breakthrough

in fronting from the NIH so very excited that we have a planning grant to potentially get this thing moving so P tract is basically designed to be a randomized control trial of catheter directed therapy versus no catheter

directed therapy for sub massive PE to really try to answer this question just like the pytho trial tried to do for systemic thrombolysis in the setting of catheter Ida thrombolysis and this time we're not just using surrogate endpoints

we're not you the rvw ratio is probably not even gonna be calculated but what we want to know are these are patients doing better in one arm or the other and we're going to use outcomes that are important to both patients and providers

400 to 500 patients most likely looking at sites all across the so but we are still in this time when

I would like to convince you that

claudication is a different disease than critical limb ischemia even though it's the same on you're lying principle it's a different disease and here's why what is the fate of a Claude account so in five years

most Claude Akins are stable now I'm not saying they're living without pain I'm not trying to diminish their symptoms they may say look I can I can't live my life because I'm you know it hurts to walk from here to there and I'm sorry

but at the end of the day most of them will be stable they're not gonna dot they're not gonna get worse and they're not gonna have an amputation only a small percentage progress to critical of ischemia now let's look at the fate of a

critical limb ischemia patient in one year the majority are either dead or have another amputation have a bilateral heba have lost one of their legs and a lot of them have lost both their legs and so this is a serious mortal morbid

disease in fact if you look at it compared to some cancers critical of ischemia has a worse overall survival than a lot of common cancers and when I was trained my mentor used to say CLI critical mass Kimia is cancer by another

name we just have to treat it like palliation okay and that becomes important the way we treat things so when I treat a Claddagh Kent I am really looking toward their entire life you know is this treatment worth it I don't

want to make you worse with a critical limb ischemia patient I am all hands on deck we're gonna do everything we can and why every 20 seconds a lower limb is lost to diabetes patients with rest pain or gangrene really need to see a

specialist I've asked your specialist not any vascular specialist a basket specialist who knows how to do critical an ischemia okay so I'm from North Carolina or I live in North Carolina now cardiovascular disease rates were you

know obviously toward toward the south hi here's the amputation rates we are right there in the amputation belt if you look at the dark blue they sort of along the south and into Texas and we're all in the amputation belt right now

because we're all in Texas and so we do way way too many amputations sadly over 50% of patients who have an amputation never had an angiogram so in other words that doesn't mean someone tried and failed which is at least respectable you

know at least tried it's we never looked we never even bothered now there's a lot of amputations that should if someone's septic and dying or sure or limbs unsalvageable of course yeah you don't just take the like I understand

that but that's not 50% that is a lot of patients who no-one's even bother looking so how do we make the diagnosis

they travel together so that's what leads to the increased pain and sensitivity so in the knee there have been studies like 2015 we published that study on 13 patients with 24 month follow-up for knee embolization for

bleeding which you may have seen very commonly in your institution but dr. Okun Oh in 2015 published that article on the bottom left 14 patients where he did embolization in the knee for people with arthritis he actually used an

antibiotic not imposing EMBO sphere and any other particle he did use embolus for in a couple patients sorry EMBO zine in a couple of patients but mainly used in antibiotic so many of you know if antibiotics are like crystalline

substances they're like salt so you can't inject them in arteries that's why I have to go into IVs so they use this in Japan to inject and then dissolve so they go into the artery they dissolve and they're resorbable so they cause a

like a light and Baalak effect and then they go away he found that these patients had a decrease in pain after doing knee embolization subsequently he published a paper on 72 patients 95 needs in which he had an

excellent clinical success clinical success was defined as a greater than 50% reduction in knee pain so they had more than 50% reduction in knee pain in 86 percent of the patients at two years 79 percent of these patients still had

knee pain relief that's very impressive results for a procedure which basically takes in about 45 minutes to an hour so we designed a u.s. clinical study we got an investigational device exemption actually Julie's our clinical research

coordinator for this study and these are the inclusion exclusion criteria we basically excluded patients who have rheumatoid arthritis previous surgery and you had to have moderate or severe pain so greater than 50 means basically

greater than five out of ten on a pain scale we use a pain scale of 0 to 100 because it allows you to delineate pain a little bit better and you had to be refractory to something so you had to fail medications injections

radiofrequency ablation you had to fail some other treatment we followed these patients for six months and we got x-rays and MRIs before and then we got MRIs at one month to assess for if there was any non-target embolization likes a

bone infarct after this procedure these are the clinical scales we use to assess they're not really so important as much as it is we're trying to track pain and we're trying to check disability so one is the VA s or visual analog score and

on right is the Womack scale so patients fill this out and you can assess how disabled they are from their knee pain it assesses their function their stiffness and their pain it's a little

bit limiting because of course most patients have bilateral knee pain so we try and assess someone's function and you've improved one knee sometimes them walking up a flight of stairs may not improve significantly but their pain may

improve significantly in that knee when we did our patients these were the baseline demographics and our patients the average age was 65 and you see here the average BMI in our patients is 35 so this is on board or class 1 class 2

obesity if you look at the Japanese study the BMI in that patient that doctor okano had published the average BMI and their patient population was 25 so it gives you a big difference in the patient population we're treating and

that may impact their results how do we actually do the procedure so we palpate the knee and we feel for where the pain is so that's why we have these blue circles on there so we basically palpate the knee and figure

out is the pain medial lateral superior inferior and then we target those two Nicollet arteries and as depicted on this image there are basically 6 to Nicollet arteries that we look for 3 on the medial side 3 on the lateral side

once we know where they have pain we only go there so we're not going to treat the whole knee so people come in and say my whole knee hurts they're not really going to be a good candidate for this procedure you want focal synovitis

or inflammation which is what we're looking for and most people have medial and Lee pain but there are a small subset of patients of lateral pain so this is an example patient from our study says patient had an MRI beforehand

that was one example so these are there have a lot of potential complications reperfusion pulmonary edema is a very very big potential complication so you could get through the case patient does

great you open up multiple pulmonary arteries and then they start coughing up blood and then they end up started drowning in their own blood and the ICU so we do not want to push that and the initial papers that you can see down

below on that table they had a very high almost 10% in some cases pulmonary edema requiring treatment requiring patients being put on CPAP or being intubated and that is because they treated too much at one time

and so now as this when this first started in the early 2000s the operators were treating multiple segments at multiple times at one time and they were using large balloons and we figured out that that was what was killing patients

and so we changed our treatment so this is the first study that was ever performed for this it was performed by dr. Feinstein I believe this was published in circulation it was done in Harvard at MGH they had 18 patients with

36 month follow-up they all improved in their ability to walk as well as their lifestyle but many of them 11 out of 18 patients had reperfusion injury so this was the first paper and at that time it became the last paper because so many

patients did poorly but here's what they're sort of what they did and the ones that did okay they you could see that they had an improvement in the New York Heart Association classification again that just means they can walk

further they're not less short of breath and that they could walk further in 6 minutes which is again our sort of first test outcomes over time whence this has become increased so you can see that study was in 2001 and then

it kind of went away for a long time and it came back in 2012 in Japan where the most operators are there they've treated up to 255 procedures now since this slide was made we're up to a thousand in Japan and those patients are doing very

well but you'll notice that they have multiple procedures so again you don't try to one-and-done these patients they come back four to six times we've treated a couple patients where I work and we've treated that was patients four

times already and so they do much better but it's a slow slow and steady treatment so I want to wrap up with saying that the IR team is very critical to patients who are getting treated for PE we're involved in the diagnosis as

the radiology team acute and chronic PE it's very important to know as I've shown you in some of the examples and some of the images which when it's acute and versus chronic doing thrombolysis on a patient with chronic PE is useless all

you're doing is putting them at a risk you're not going to be able to break up that clot it's very important to have inter and multidisciplinary approach to patient care so interdisciplinary meaning everybody in this room nurses

technologists and physicians working together to take care of that patient that's on your table right now and multi-disciplinary because you have to work with cardiology vascular medicine the ICU teams and the

referring providers whether it's neurosurgery vascular surgery whomever it is who's Evers patient gets a PE you have to work together and it's very important again to have collaborative care in these patients if we're doing a

procedure and somebody notices that the patient is desaturating that's very very important when you're working in the pulmonary arteries if somebody notices that the patient's groin is bleeding you have to speak up so it's very important

that everybody is working together which is really what we need to do for these patients so there's my references and there's my kid so thank you guys very much hopefully this was helpful I'd be

note of PA D in patients with diabetes unfortunately in diabetes all the bad things that happen in PA D amplified in diabetes so 20% of patients with

diabetes over 40 40 have PA D diabetes increases the risk of claudication three times in men eight times in women all right basically everything you think about going bad happens in diabetes it is more common it's more often silent

which means you're not going to catch it earlier it happens at a younger age it gets worse faster and the male and female distributions equal 15% of patients with diabetes develop ulcers and 85% of amputations it's the most

common cause of non-traumatic amputations worldwide and should be preventable so when we're in the angio

so I'm gonna show an example this is a 57 year old male who presented with a dis neo

he had World Health Organization functional class 3 meaning it's significantly affected his life he can't walk up the flight of stairs really tired walking from the parking lot of his favorite restaurant back to this car

can't really walk around the grocery store he had a history of DVT and PE also had afib he actually went to the ER and was diagnosed with upper respiratory tract infection which many of these patients are they've put him on

antibiotics then for pneumonia he had a VQ after one of his doctors just felt like he just wasn't getting better and it found multiple mismatch defect I'm sorry I don't have those pictures he was actually started on home oxygen after

all of that work up it was found that he had CTF and this required I think three different hospital visits and every time got kicked up to sort of a higher acuity place and then he ended up at our place so these are his pulmonary angiogram

images here I don't know if I can play these but the still images kind of show you that the images on the right show that there's basically no vessels going out distally so I mentioned pruning of vessels there's no branches in the right

upper lobe if you look at the right lower lobe at the tip of the catheter there's areas of stenosis right where the segmental arteries start and on the left you can see that the left pulmonary artery is denuded essentially the entire

left upper low branch is excluded by a rim of thrombus and in the left lower lobe the image on the bottom my bottom right there's actually no branches going to the left lower lobe into the lingula so this is a patient that has had very

bad CTF their main the pulmonary artery pressures are listed there of 77 where the normal high is 25 so three times the normal pulmonary artery pressure so this patient went on to an operation so the image on the right the photograph is

actually the clot that they removed from the operation and that patients pressures improved from 77 to 22 immediately after the operation so they go to the ICU they have a swan-ganz catheter left in place and you can

measure their pressure right afterwards and you can see that that clot they grabbed it it looks like a bunch of fingers well what they do is they crack the chest open like with a mini sternotomy they make an incision in the

pulmonary artery after they put them on bypass and then they basically grab they use they're a little deBakey's the DeBakey forceps and they grab this little elevator and they just start scooping

out the clot and they try to grab it as one big piece take it out and then you get that nice photograph on the side if they break off pieces it's actually worse because that's an area that a pulmonary artery dissection can occur so

it's a very complex operation but you get very nice results and afterwards these patients are sent home usually on lifelong anticoagulation thereafter so

guys do so when we do our screening phone calls and our pre screens before

the actual procedure there's a few factors that we look at for the patients with blood pressure the patient needs to be vitally stable before we do a procedure there may be a slightly increased risk of bleeding for kidney

biopsy if patients are hypertensive although it hasn't been noted to be statistically significant in the literature so we are always aware of patients being hypertensive we do want them to be taking their medications the

day of the procedure we also do a full medication reconciliation with the patient making sure that we're checking on any anti platelets anticoagulant medications and we have a list of our hold times that we use for a reference

we already discussed for those of you who are at this session this morning the issue of liver disease is it stable liver disease they may have adequate he stasis even though their INR is not within the normal range and so we

recommend a stable INR of less than 2.5 for those patients and in our practice a lot of the providers are going away from correcting the INR s for our patients we also screen for hematological disorders do they have some known condition that

makes them more likely to bleed or conversely more likely to clot and that may factor into whether or not anticoagulation can be held do they have a current diagnosis of cancer are they going to be getting one of those

angiogenesis inhibitors might they have thrombocytopenia and we just do a brief review of the patient's chart before we call them to kind of look for those diagnoses do they have a history of bleeding especially if they have no one

platelet dysfunction you know a known history of bleeding can be a reliable predictor of bleeding risk for some patients and do they have a cardiac or a neurological history as we learned this morning patients that have recently had

a cardiac stent placed we can't just say yeah stop your plavix hold off 5 days it'll be fine that could be a very serious risk to the patient did they recently have a stroke have they had a PE why are they on their anticoagulation

if they're on it so we really need to be aware of the whole patient and having that pre-screening phone call with them can allow our nurses to figure out a lot of these problems and then alert the radiologists and try and troubleshoot

before the patient walks in the door and says yeah I took my warfarin this morning I'm all ready for my liver biopsy the radiologists don't like that much in it you know it's really a bad thing for our high volume area to have

that happen and this is just another chart of our oh did I get mixed up here you guys are gonna fire me from running this clicker there we go so the whole times are again based on the half-life and the mechanism of action and this is

pretty similar to what you saw in the the presentation earlier today and specifically that imbruvica that's something that we alert the radiologists who they have a discussion with the patient decide is this something that we

want to continue with and I will say that in our practice with the volume and the the level of acuity of our patients I think that a lot of our providers are fairly comfortable with a certain level of risk because that's just who our

patient population is you know we have a very large hospital two large hospitals and very sick patients so that's something that we you know some of them are more comfortable than others but it's a risk-benefit thing that they have

to decide on themselves with the patient obviously all right so here are our

I want this to be as instructive as possible I do have some multiple-choice questions that are peppered in there and hopefully you guys feel comfortable enough to shout out answers I really don't care if you get it right or wrong so but if I teach it right I hope it's

clear what the answers are okay so and and I know the title test says that I'm going to be talking about parts frankly I think there's a lot more to talk about about PE other than parts and I'm not going to be emphasizing that

but if there's time to ask questions or I'm happy to speak about that as well because I think the disease and the treatments are really the crux of PE at this point okay so I start with something called the landscape where are

we with pulmonary embolism well you know I don't know how many of you have seen PE in the IR suite or have dealt with these patients or even have friends or family that have had a PE but I don't think anybody who's interacted with this

disease would argue with the fact that PE is a big deal why do I say that statistically speaking well there are 900 000 VTE events per year that's DVT or PE that's a lot it's almost a million now the number of deaths from PE every

years quoted to be as high as 300 000 but is around 60 150 is what we think so quite a few this affects everybody you know you might have heard of Serena Williams getting a PE Chris Bosh and Serena Williams I think had a massive PE

which I'll tell you the definition of that later but it's a it's it's something that can affect a young person and kill that young person so that's what makes it a little bit tougher than some of the other diseases it's the

third most common cause of cardiovascular death stroke mi then PE ten percent are fatal within the first hour so a lot of these patients you're not even gonna see and when you do see them you've got a big task ahead of you

because they're you're trying to rescue them from death that's basically the same statistic now if you were to take every patient who comes into the hospital and you put an echocardiogram on them and you looked at the right

ventricle their right ventricle would show some evidence of dysfunction and so that's an interesting statistic because right ventricular dysfunction is you'll see on a subsequent slide is actually a pretty big deal and is actually at the

crux the pathophysiology of PE now if you were to do a VQ scan around six months after people got a PE you would find that 1/3 of those patients actually have residual thrombus so we think that you

know PE is a acute disease but what we're finding is that it's actually a cute disease that can become chronic and a lot of people and we're actually revealing unveiling the fact that maybe a year or two years after their PE these

patients aren't doing as well as we thought so that this is a burden it's a chronic it's a chronic disease that causes a burden on their lives so this is the disease and and you know as an IR you look at this and you say well that's

pretty exciting looks like we can intervene on something meaningfully but there are some caveats we should remember first most patients have low risk PE s I'll define that in a little bit but these patients don't need an

intervention they just need anticoagulation to the best of our knowledge that says all this this group needs sub massive PE I'll spend quite a bit of time on and it's a very controversial topic and there's a

lot of different attitudes between interventionalists and non interventionists about sub massive PE when you get a massive PE patient this is the patient that's crashing and burning most of them should receive

systemic thrombolysis which is an IV in the arm and a drug through their vein it's the fastest thing you can do and it doesn't involve corralling an IR suite the team for the IR suite or a surgical team and as I just said there's a wide

range of attitudes regarding treatment aggressiveness so I'm not going to go

do we care about carotid occlusive disease why is it such a big deal stroke is a major factor obviously stroke is the third leading cause of death 750-thousand approaching a million

strokes a year and it's a leading cause even if you survive the stroke of disability majority of these are ischemic and not bleeding or hemorrhagic strokes and a lot of them a significant number of the ischemic strokes reside or

source from carotid disease so the carotid is the issue in those patients and the stroke risk in those patients is as ultimately related to the degree of stenosis that they have or narrowing that they have at the carotid and do

they have any history of neurologic symptoms that determines if they're symptomatic or asymptomatic so you could have a critically narrowed lesion but have zero symptoms that's asymptomatic and you can have a

less significant so no --ss not 99% but say 70% but you have some symptoms you're getting blindness intermittently or or intermittent numbness in your hands and that's symptomatic right and with

that that's a much more worrisome sign in the setting of that even though milder stenosis so what is the you know the importance of this is for us to be able to to determine which patients who we would be treating or not so we're all

these are our prospective CDT trials it's a lot to go through them so I'm not going to suffice it to say that the only one of these that is randomized is the

one in the top left the ultimate trial with 59 patients the rest of these are single set are single arm studies the optimized trial was randomized but the key arm it did not have was a control arm so all it did was vary the amount of

drug but there was no control arm to tell us how are people doing if they just get heparin well and I'll show you one result from these trials that is the most important result and that is up from the ultimate trial at 24 hours CDT

catheter to thrombolysis reduces the RV to lv ratio to a greater extent than heparin alone what does that mean so you saw all those pictures with the big dilated right ventricles our surrogate measure for right ventricular

dysfunction is the ratio of the diameter the inner diameter of the right ventricle to the left ventricle what we found in this study was that that ratio got reduced to a greater extent at 24 hours in the CDT arm compared to heparin

alone that means that CDT seems to reduce our V dysfunction faster than heparin now importantly 30 days later the echos looked identical so really it's a question of time which is not surprising what we've noticed in

our practice is that patients feel better faster okay I'm gonna go through the rest of this because I'm out of time but I want to give you a little bit of a sense of where we're going because there's bleeding associated with CDT and

maybe I'll show you this that in the Seattle to trial there was an 11% major bleeding rate now this was a pretty conservative definition but there were some serious bleeds and there were no intracranial

hemorrhages in this study but we have realized that CDT is not risk-free it's not like we've all of a sudden gained all of the advantages of systemic thrombolytics and none of the disadvantages now the rate of

intracranial hemorrhage seems to be about tenfold less but it does happen about 0.2 to 0.4% of the time the rate of major bleeding seems to be about 5% which is about half the rate of major bleeding that we see with system or

thrombosis so bleeding is still there it just doesn't seem to be as frequent so that's where some of these other devices are coming in then our a float Reaver the the the extra penumbra indigo cat 8 device and so the the float Reaver is

has actually gone through the full trial and the results are about to be published what is this thing well it's this pretty big hose which is about 20 French and it goes through the right heart and goes up there and it takes

this clot and literally aspirates it out and these are some of the things that will come out and that's sort of your post picture right there the data showed something similar to what we saw with the catheter directed thrombolysis

trials they had looked at 106 patients are vlv ratio was reduced again there's no comparator arm here so this is just the device on its own with a 3.8 percent adverse event rate and so now we're talking about mechanical devices that

don't use a clot-busting medication therefore you're gonna you can expect less bleeding but you're trading some of that off for a mechanical device that can cause injury to either myocardial structures or to the pulmonary artery so

that's something we have to be highly cognizant of as they're introduced into the market this is the penumbra cat 8 this is from Jim Benenati publication basically showing a couple things that's the separator that is the actual

catheter and that's the sheath back there so you've got poor profusion because of a clot in the inter lobar pulmonary artery and then at the end of it you have better perfusion for lung down there so we actually just completed

enrollment into the extract PE trial 120 sub massive PE patients the same efficacy endpoint you have to remember that has been established by the FDA as a way to get approval this is not the final

study nor should it be the final study when we evaluate these devices so to summarize sub massive PE what does the data not tell us CDT probably reduces the RV to LV ratio at 24 hours that is the main outcome that I want you

guys to remember from the ultimate trial it's associated you didn't see this data so don't worry about that we do see major bleeding and sometimes rarely but sometimes we see intracranial bleeding with CDT as well so what we're missing

from catheter directed thrombosis for sub massive PE is what are the clinical outcomes the RV to LV ratio is a surrogate outcome what about death what about clinical deterioration what about recurrent hospitalization what

about recurrent VTE how are people doing in the long term are they walking as well as they were before we don't know any of this none of the data right so far can tell us any of this information so where do we go from here for sub

peripheral artery disease affects up to 12 million peopl amputations occur yearly do a peripheral artery disease specifically critical

limb ischemia that is almost certainly way more than should be done up to two million people have critical limb ischemia so how do patients present when they have PA d in general okay there's really one of two presentations general

categories the first thing is intermittent claudication so Claude occation means I walk and I get pain okay when I stop walking the pain goes away you also have critical limb ischemia

which we call CLI CLI is such severe peripheral artery disease that you actually a foot and leg pain at rest in other words your blood flow is so bad that even at rest you don't have enough perfusion to go to

your foot and you have a scheming pain or your blood flow is so bad that you can't heal a sore or an ulcer okay so forget walking these are the this is the most severe form of peripheral artery disease

okay so again Kumar mentioned this before peripheral artery disease is like a highway if you and I say this a million times a day my pas are so sick of hearing it if you block a highway traffic can't get through and so it has

to go through detours when you go through detours you're always slower things are never as efficient and you back up that's exactly what happens here plaque builds up in the artery blood flow can't get through and so you can't

get to where you're going there's the highway analogy a key point and again I hear this all the time you know the patient came in with a wound but it's weird they never had claudication so maybe this isn't arterial wrong

intermittent claudication does not need to come before critical limb ischemia in other words many patients their first presentation is critical of ischemia so they'll never know that PA D they never have what you know pain when they walk

their first presentation is a potentially severe morbid and mortal one so what are the risks factors for PID it's everything we think about smoking obviously is a big one high blood pressure cholesterol diabetes obesity

physical activity well there's other risk factors family history and age so my question is what's the difference between these two risk factors what there's been these risk factors and these risk factors

one is changeable the other is not as much as we try with Botox or Juvederm or whatever it is we can't change our age and as much as we try we can't change our family history but we can change smoking and cholesterol and do all the

things that we can do and it's not easy but it can be done I will say a special

briefly mention this because dr. sista

is gonna talk more about this on Tuesday but this is a slide from MGH where they started the pulmonary embolism response team and this is sort of how things used to be and I think most hospitals across the country and still exist in some

places where a patient shows up with PE and then about 20 different teams are consulted and kind of wait for everyone to say what they think you know vascular surgery may if they're involved may say something cardiology is gonna say one

thing ir is going to be involved and say something the critical care teams are going to say something and you're waiting for everyone to sort of get consensus which you may actually never get and all the while a patient is

sitting in the ER finding it difficult to breathe maybe probably an oxygen maybe not on a heparin drip and then what are you gonna do with that patient well what's the right treatment and then where are they going to go afterwards

and how are we gonna monitor them in their future well after the pulmonary embolism response teams have started showing up throughout the country it's a much more streamlined process patient shows up with a knee to the ER at our

institution a page is sent out after they're seen by the ER team and that involves a medical team usually vascular medicine or the pulmonary critical care IR interventional cardiology if they're involved the critical care services and

whatever whatever service initiated that and then it sort of goes through that process where the patient gets gets a consult from a multidisciplinary team much like a tumor board and we make a general consensus in our institution

this happens within 30 minutes of the patient hitting the door at this point so there's no longer like a two or three-hour wait to make a decision it may not always be the right decision but if that patient for example gets worse

over there the next two hours if we decide we're going to just treat them with anticoagulation and oxygen and telemetry in 30 minutes they may get worse and then we have another call and we make another decision and then we may

say you know what push TPA or they need to come to IR to get a catheter based intervention and again dr. or sisters can talk more about this but it really helps us with disposition and treatment

common it's great

incidents of patients and up to a million a year in Europe about 200 about from PE so there are more deaths in the

P from PE in the u.s. than aids motor vehicle accidents and breast cancer combined so it's a very high cardiovascular more rate it causes about 15% of all in hospital deaths as well it's seen in 40

to 50 percent of patients with symptomatic proximal DVT so in the above the knees so the femoral veins popliteal veins and iliac veins and recurrent PE is a very substantial risk a lot of patients have missed diagnoses of PE so

they come into the hospital with some chest pain shortness of breath maybe a light a low-grade fever they're seen in the ER and then they're thought that they maybe have pneumonia they have a viral bronchitis and it turns out that

they have pulmonary embolism so the

talk here with something that's new on the horizon believe it or not it was actually on the horizon 20 years ago and then it went away because there were a lot of patients that were treated with a

lot of complications and it's making a resurgence and this is balloon pulmonary angioplasty or BPA for short so this is an intervention which may be feasible in non-operative candidates so I mentioned to the Jamison classification earlier

type 1 and type 2 disease should be treated with surgery again it should be treated is curative but patients with type 2 and a half or 3 disease can be treated with balloon pulmonary angioplasty in the right in the right

frame which means that a surgeon has said I cannot operate on this a medical doctor has said boy they're not going to get better with their medicine let's try something else well this is that something else and that's what involves

everyone in this room so this is these are usually staged interventions with potentially high radiation and contrast dose if you think about it it's like Venis recan and a pulmonary AVM all-in-one so it's a potentially a long

complex procedure with a lot of contrast and a lot of radiation but it can provide a lot of benefit to these patients I'm going to talk about the comp potential complications at the end which is one reason why not

everyone should do these all the time so this is a pulmonary angiogram from the literature when you're injecting a selective pulmonary artery you can see that this patient has multiple stenosis there's no real good flow there the

vessels look shriveled up like I mentioned to you before you can get a balloon across it and balloon the areas and then you can see afterwards so the image a on the left is before an image D is afterwards believe it or not this are

in the most experienced hands because the most experienced hands are for palm the BP AR in Japan they do hundreds of cases of these a year at each hospital I've personally only done five so but this is a something that I'm very

interested in and you can see how how much benefit it has for that patient another way you can see these are the webs and the bands that I mentioned to you earlier so what's interesting is that if you look on the first set of

images on the top and the images on the bottom those are the same patients it's the same view before top rows before and the bottom rows after balloon pulmonary angioplasty so the first image is a pulmonary angiogram where if you kind of

see this there's there's some area areas of haziness those are the webs and bands the image on the the middle is the blown-up views and you can see those areas and then the image on the right is intravascular ultrasound which I use

every day in my practice it's a catheter with an ultrasound on it and when you look at it on the top image image see you can see a lot of thrombus you're actually not seeing flow and on image F on the bottom you're seeing red which is

the blood flow so these patients can actually improve the luminal diameter bye-bye ballooning them you can treat occlusions again image on the left shows you a pulmonary artery with a basically an occlusion proximally and then after

you reek analyze it and balloon it you can see that they can get much more

new data of the Emmy trial that came out last year our ten-year results saying

that after ten years after ten years women who wanted to retain their uterus they looked at them in ten years three-quarters of those women were still very very satisfied and also were still able to retain their uterus so ten-year

data came out randomizing people for uterine artery embolization versus hysterectomy of the women who chose you to an artery embolization ten years later they were still very happy so I tell my patients that this is what you

should expect that you will have symptomatic improvement in 12 months around 85 to 95 percent of the patients are pretty happy there is a entry intervention rate it is not zero and it can be higher than ten

depending on what kind of Imogen is seen ahead of time and that we know that dysfunctional uterine bleed tend to do a little bit better than bulk type symptoms and that's partly because of subjective nature of that so this is one

of the patients that I treated when I was in in Virginia and Riverside and she's a former miss Brazil and she came to see us with what she also called reversed cycles like she would bleed more than she would not and she was

wearing depends and it took everything to just coach her out of the car to come inside to do a consultation because she was so afraid that if she got out she would be sitting in a pool of blood and she had an MRI showing what looked like

a eleven point seven centimeter fibroid she had embolization and that was her six month follow-up MRI to the right which looks like a very impressive result they don't all look this way which is why I save this image something

that looks like a normal uterus now I for the persons that I told to hold your high horse here is the time okay so what happens if I want to have a baby because these are the things you remember we're being ambassadors for this procedure we

need to be having the answers for the things that are our friends and family members are going to be asking us so if you want to have a baby I would say that the data that informs us as to what to do with you is still very weak but the

only randomized prospective trial that we have out there says that you should actually have myomectomy and a Cochrane review was also done and it still says that there's very low level evidence suggesting that myomectomy may be

associated with better fertility outcomes as opposed to UAE but more research is needed and we still require more research so at the very least what I have to do and now you feel compelled to do is to send my patients to see

someone who is a fertility specialist in consultation so we can make this decision together so if your poor surgical candidate if you have the gazillion fibroids and if you've had surgery before a hostile

abdomen and the patient says you know what dr. Newsome there's nothing that you can tell me ever to say that I'm going to have surgery then we're going to be doing something else that is not surgery okay the other thing that your

about massive PE so let's remember this slide 25 to 65 percent mortality what do we do with this what's our goal what's

our role as interventionalists here well we need to rescue these patients from death you know this it's a coin flip that they're going to die we need to really that there's only one job we have is to save this person's life get them

out of that vicious cycle get more blood into the left ventricle and get their systemic blood pressure up what are our tools systemic thrombolysis at the top catherine directed therapy at the right and surgical level that what

unblocked me at the left as I said before the easiest thing to do is put an IV in and give systemic thrombolysis but what's interesting is it's very much underused so this is a study from Paul Stein he looked at the National

inpatient sample database and he found that patients that got thrombolytic therapy with hypotension and this is all based on icd-10 coding actually had a better outcome than those who didn't we have several other studies that support

this but you look at this and it seems like our use of thrombolytics and massive PE is going down and I think into the for whatever reason that that the specter of bleeding is really on people's minds and and for and we're not

using systemic thrombolysis as often as we should that being said there are cases in which thrombolytics are contraindicated or in which they fail and that opens the door for these other therapies surgical unblocked demand

catheter active therapy surgical unblocked mean really does have a role here I'm not going to speak about it because I'm an interventionist but we can't forget that so catheter directed therapy all sorts

of potential options you got the angio vac device over here you've got the penumbra cat 8 device here you've got an infusion catheter both here and here you've got the cleaner device I haven't pictured the inari float

Reaver which is a great new device that's entered the market as well my message to you is that you can throw the kitchen sink at these patients whatever it takes to open up a channel and get blood to the left ventricle you can do

now that being said there is the angio jet which has a blackbox warning in the pulmonary artery I will never use it because I'm not used to using it but you talk to Alan Matsumoto Zieve Haskell these guys have a lot of experience with

the androgen and PE they know how to use it but I would say though they're the only two people that I know that should use that device because it is associated with increased death within the setting of PE we don't really know you know with

great precision why that happens but theoretically what that causes is a release of adenosine can cause bradycardia bradycardia and massive p/e they just don't mix well so

individually into each one of these trials but I want to just point out to you how busy the last 5 years have been because it has really caused a

resurgence in our interest in both treating PE better and what the gaps are in our knowledge so I will point out in 2014 this was an inflection point for 10 years we didn't have a major trial actually more like 12 or 15 years we

hadn't had a major trial in in PE and pytho was a 1000 patient study that informed us about how systemic thrombolytics interact with sub massive P and I'll go through the data that same year

catheterized thrombolysis is everybody familiar with catheter at the thrombolysis for submasters before Pease that's totally off the grid okay good well this was the first time we had a randomized trial for catheter directly

thrombolysis with some with some massive PE only problem was it was 59 patients in Europe so and that's all we have as far as randomized trials for CDT this is my soapbox issue I'm sorry if you've heard me say this but that's that's my

big goal is to try to change that 2015 had some follow-on CDT trials 2017 this is when we started thinking about the long term effects of PE on patients both of these studies started to examine the issue where a year after the PE patients

are not normal if you did a for example this elope long term study almost 50% of patients had an abnormal cardio pulmonary function test one year later 2018 we started to experiment with the dosage that we're

administering during CDT that's the optimized trial and we saw the first trial completed for a mechanical device called the NRA flow trailer which I'll show you later in the talk as well so that was an exciting inflection point as

well the extract PE trial which uses the indigo cat 8 device to aspirate thrombus in pulmonary embolism we just completed enrollment this year the future is hopefully bright for generating more data the PERT consortium registry is up

and running and is hopefully going to help us aggregate data and make better decisions and then you have a couple more devices coming in and I'll tell you our efforts to try to really improve the knowledge base on what CDT for sub

massive P that's the P track trial that's the last bullet point there okay

a little bit more systemic versus catheter directed thrombolysis so once you've decided that a patient needs TPA what are the differences here well if

you give patients systemic TPA you're gonna give them a much more rapid delivery this is for those patients who have high-risk PE they're the ones who are coding for those patients you give them 200 milligrams of IV usually you

get 50 first and then another 150 over a very short time period they have a very high risk of bleeding as a result of that a catheter is much slower you're gonna infuse one milligram maybe which is what I think most people do

over several hours maybe a few maybe a day so it's slower targeted versus non targeted well catheter is much more targeted you're gonna give Pete you're gonna give the TPA right into the

pulmonary arteries that's the whole point in our in our thought process as a result you give a lot less drug so when you give a patient based off of some of the trials 24 milligrams of TPA over a 24-hour period that's a lot less than

200 milligrams in a 10 minute period and then the bleeding risk is very different for these patients catheter based treatments have a high bleeding risk but it's possibly lower than the initial bleeding risk of patients getting

systemic TPA so I wanted to go through a

we're gonna gonna talk this morning about pulmonary embolism and acute and chronic PE and try to put in a lot of information regarding imaging and interventions I want to start by thanking the avir Board for inviting me and the AR Rin board today as well and

of course Sam for organizing this wonderful meeting and she is one of my favorite Tech's so I also like to acknowledge a lot of people so we all have mentors in our career David Williams is one of my mentors dr. Barnes

helped us at Michigan start up our pulmonary embolism response team and since I'm talking about PE so it was great to talk about that a lot of what I talk about today is gonna be followed up with another talk on Tuesday from dr.

okey sister who's one of the world's experts at PE and so he's going to talk about managing care as well and of course to our excellent team of nurses technologists residents fellows will all help take care of patients every day so

I always like to start out with a patient so the first for our first case today it's a 54 year old male who had a prior history of a stroke hypercoagulable condition and known no known prior DVT

and PE he had increasing shortness of breath for about three days his heart rates were in the 90s to hundreds he had okay blood pressure in the 120s he had a CT that confirmed sub massive bilateral upper and lower low Pease with

right ventricular strain and then the RV strain was also seen on a TT II and had elevated cardiac enzymes so this is a very typical patient here's an image on the CT on the left and on the right showing that the patient had a large

amount of pulmonary embolism and I'm sorry I don't have a mouse to control that but in the right upper and branch points on the left you can see that there's PE so pulmonary embolism is very

CT scan frequently or they actually show up with a CT scan so I want to highlight the fact that this is different these images are different than the patients

who had acute pulmonary embolism I will say that it's very hard to kind of get this into your brain but they're very different so first of all they'll have a VQ scan that'll show that they have mismatch defects after that when you

look at the scan the clot has a different appearance before it was in the middle of the vessel it was surrounded by a rim of normal contrast here it's actually wall adherent it's irregular it's got weird weird angles to

it weird margins and then distally the vessels are very small in acute PE the proximal pulmonary arteries are enlarged because they're hitting they're enlarging because they're hitting a roadblock in here in chronic PE the

vessels shrink down and shrivel beyond it because there's chronic clot they're a lot like patients who have chronic DVT in their legs when you look at that sagittal view kind of think back to the original case that I showed you

you saw that sort of with clot there's a thin lines floating in the middle of the vessel here it's irregular it looks serrated it's gotten really weird angles so this is another example of chronic PE from the literature that believe it or

not is not mediastinal adenopathy it's not a patient with cancer it's a patient with chronic PE all that thrombus sort of lines the inner walls of the pulmonary arteries you can even have calcification just like you would have

in atherosclerosis also the vessels distal to the clot become shriveled down and that's a way to tell if that's chronic PE versus acute here's another example of a patient of the image on the left is the patient years or before and

then the image on the right is a patient with chronic thromboembolic pulmonary hypertension and then a few more examples showing you that it's usually on the side of the blood vessel rather than in the middle of the blood vessel

so if you want to know just an easy way if you see clot in the middle of a blood vessel it's probably acute if you see it on the side and along the walls it's chronic more pictures kind of just to put in your brain so the diagnostic

much more controversial so you it was pretty clear that we have to rescue

massive PD patients from death but with these statistics what are we supposed to do with sub massive PE well are we supposed to prevent mortality it's gonna be hard to do if the mortality is only 2 to 3% because you're trying to really

improvements of a very low statistic are you trying to reduce the rate of hemodynamic deterioration that's a possibility what about long-term disability if you remove clot upfront

will these patients do better six months one year or two years down the road frankly we don't know the answer to any of this and the reason is that the pytho trial made things quite difficult for us to interpret the pytho trial was the

trial that was going to answer all uncertainty this was a trial where it took some massive PD patients in that high-risk intermediate category and randomized them to receive a bolus of tenecteplase which is similar to TPA but

is not the same versus anticoagulation alone what did it show well it showed there was no difference in death between tenecteplase and placebo so they actually gave a placebo drug so that no it was a double blinded

study now if you look at the next line though a lot more patients decompensated if they receive the placebo than that's not to place this is not a bad thing you know it's not it's not great when you have to intubate somebody or initiate

pressors so if you can avoid that outcome that's it that's a pretty good thing so maybe it is the right thing to give systemic thrombolysis in the setting of sub massive PE problem was this the bleeding you look down here

there was an eleven percent rate of major bleeding in the tenecteplase arm there was a two percent rate of intracranial hemorrhage so now we've got this therapeutic window that's hard to interpret so we seem to be improving

outcomes from an efficacy standpoint but then we're also increasing the rate of bleeding so basically what we've sort of coalesced around is that systemic thrombolysis has a questionable risk benefit profile because the rate of

bleeding and the rate of really serious bleeding is makes us nervous so is that an opportunity for catheter director thrombolysis and I'll call this the poster child for Catherine throwing license if this is how it worked every

time we might have a homerun so this is gentleman looked terrible well still in the sub massive category but breathing at 35 times a minute hypoxic had his main PA systolic pressure of 60

millimeters of mercury you look over here and there's this large clot in the right upper lobe go to the left side and then there's all this clot in the left lower lobe as well so what do we do we put in bilateral infusion catheters this

can be an E Coast catheter it can be a standard catheter these areyou nafeez catheters have side holes starting from here and ending it's hard to see but there's another radiopaque marker somewhere down there on this side there

and somewhere over there and between those markers you have multiple side holes and those are put up inside the clot so you're dripping TPA at a rate of about 0.5 to 1 milligram per hour and you're getting it directly into the

clock that's the theory and so after 20 to 24 hours of that you know you're given 20 to 24 milligram of TPA that's compared to 50 or a hundred that you get was sitting with systemic thrombolysis you get something

that looks like this where the pulmonary arteries look pristine the PA still the systolic pressures come down the patient feels great now the skeptic would look at this and say well if you just tried some heparin and you just infuse saline

would you have the same result and frankly if you were to conduct the experiment you might find something interesting or not interesting but we never have conducted that experiment but you know I'll tell you a little bit

about the ultimate trial if I have time I don't want to go to overtime though

of critical of ischemia well a lot of times it starts in our office with a physical examination so we do a risk

factor assessment and this is what happens before they get on our table with with everyone in this room and us seeing the patient assessment of intermittent claudication and it can be subtle many patients don't come in and

say oh yeah I have pain when I walk for a short time and then it I rest and it goes away a lot of times it's yeah you know my leg gives out or now it doesn't hurt it's kind of this weird feeling when I walk and it these atypical

symptoms and then obviously if they have a wound you have to a wound evaluation on physical examination things we're looking for feeling a pulse you'll be surprised how many primary care providers never feel a pulse and if we

say if you feel a pulse you may save a life because you may be the first one to say hey this patient doesn't have a pulse maybe they have got peripheral artery disease and if they prefer order these maybe have coronary artery disease

and maybe they should we start on aspirin or statin and save them from a heart attack and stroke and so you really can save a life abnormal capillary refill so in other words you've got such bad blood flow

that if you smush on their foot it takes a long time for that blood to come back because they have such poor perfusion there's something a Peugeot stess TWEN that if you lift their leg gravity alone pushes their blood isn't it overcomes

the force of blood and so there are foot becomes power becomes losing some color and then when you put them down it dilates and you get sort of this ruborous red color so that's a burger sign I just had a good example in clinic

about a week or two ago so what do we ask for patients do of any pain or discomfort in the leg thigh or butt with walking your exercise I will sell you tell you I often don't use the word pain because everyone thinks pain is

different so so some people say well it's not paying it's a key lake ease pain to me I'm a guy everything's pain to me right low low threshold but discomfort is a good way of asking it foot or toe pain

that disturbs your sleep do you have any skin ulcers or sores on your ankles feet or toes I think it's very important to know what kind of patient you're talking to in terms of Education level or in terms of just language so some patients

don't know what it all sir is and they use the term sore some people don't know what a sore is they used term wound and so just sort of you ask things different ways I think is really important when we all talk to our patients and again a lot

of classic history will miss a large majority of PAE because patients don't read the textbook the one thing I'll say is I hear this all the time well the patient had pulses and so they don't have P ad that is hashtag false and the

reason is pulse exam is insensitive so in other words even if you feel pulses they can still have peripheral artery disease okay now if you don't feel pulses they certainly have peripheral artery disease or you're just terrible

at it PID classification the way we talk about patients with PA D we use a classification scale called Rutherford it may come up so in other words patient who has PA D but asymptomatic is

Rutherford zero a patient who has got major tissue loss and is basically 1 for amputation is Rutherford 6 and then everything in between is sort of a gradation we cut off 3 to 4 so 3 is claudication pain only 4 is critical in

ischemia rest pain alright so rather for classification when we talk about wounds you may see this you don't need to go in details but there's a Wi-Fi classification that sort of Germans how bad is the ulcer and how likely are you

to to lose your leg it's sort of a prognostic I will remind you that in medicine there's differentials for everything in other words the patient comes to you with pain or you talk to your friend or whatever with pain

there's a lot of things in cause pain it could be back pain arthritis infection DVT so there's things we have to think about when I was in medical school I sort of loved this my OB GaN professor said when he sees a patient the first

thing he does is say what do I think this patient have if this were a man because you get so pigeon-holed in your specialty every patient we see as well must be vas here must be vas care but you've got to take a step back and say

okay well am I missing something maybe it's arthritis may something else so don't get pigeonholed by your own prejudices which is a good life lesson in general there's also a differential for wounds so obviously

when we see a wound we could have arterial arterial tends to be sort of the toes and distal foot it can be severe pain if you see an ulcer around the ankle that tends to be more venous so vein related which again we

can treat and then a common cause is neuropathic so if you see I'm sort of at the pressure points where people walk a lot of times patient diabetes will step on something and where you and I would be like oh man that hurts

I better oh my god I have a wound there I better check that out they'll never know because they don't feel their feet and so they could have this monster ulcer and finally someone inspects their feet and says you know you have like a

golf ball sized hole in your foot and that's the first time they ever notice it so how do we test ever for peripheral artery disease well a lot of it is non-invasive now we do a B is a b is is a measure of blood pressure in the foot

or leg we can do some ultrasound to actually look at the artery and obviously we can do CT and MRI when we look at ultrasound you may look at this every once a while this is a normal ultrasound Doppler waveform where we've

got good blood flow up down and back three now the reason that's important is that correlates the sounds so if you listen to a artery i'ma do my best Doppler impression out okay a normal artery goes once you start getting

peripheral artery disease you lose that triphasic waveform it becomes biphasic when you get severe peripheral artery disease you lose that biphasic waveform it becomes monophasic and when you have nothing it becomes

okay so here's want to be alert to that so ankle brachial index is important and it's helpful again some patients who have calcific us a-- fication it's not helpful for I will tell you a B eyes alone actually not only do they predict

PA D they predict death that's how important PA D is link to mortality CT and MRI is very useful you can see here we can see a good anatomic description of the arteries unfortunately patients with calcium

sometimes we can't see as well because the calcium is so bright on CT scan that it obscures the lumen so we have other problems in patients with diabetes and heavy calcification and a lot of those patients just need to go to angiogram

and as you know my techs and nurses know sometimes rarely but sometimes we do an angiogram and it's normal and we say or there's mild disease we say okay perfect we've taken that off the table we need to move on when some of these

non-invasive testings aren't as clear so alright so in summary critical of ischemia is a morbid disease and can be the first presentation of PA d clinical suspicion and accurate diagnosis is essential for early diagnosis and

treatment and a multidisciplinary team that includes vascular venture loss who know critical limb ischemia not just the SFA and iliac artery jockeys and wound care specialists do decrease amputation rates I like this quote it's not mine

but I'm going to steal it with impunity amputation is not a treatment option it is a treatment failure okay so we have to keep that in mind I appreciate everyone's attention because we can save questions to the end or you do it now if

there's pressing I think we may need new batteries or my thumb's weak which is also a possibility any questions

that's background let's talk about what I mean when I say massive sub massive low risk high risk intermediate risk low risk all these definitions they're

actually pretty precise and so I think we need to be on the same page for that so when you see this what do you call it saddle saddle is a reasonable one large because there's I'm not sure automatically did that but would you

call it a massive PE how many would say yes this should be called a massive PE okay how many no okay it's not a big deal I'm not remembering faces but this is not necessarily a massive P I'd be surprised

if it wasn't but it's not necessarily because I haven't given you a key piece of information the hemodynamics massive PE is all about hypotension so what does that mean so this is from the American Heart Association in 2011 a massive PE

is an acute PE with sustained hypotension meaning a systolic blood pressure of less than 90 millimeters of mercury for greater than 15 minutes or requiring inotropic support okay so doesn't matter where the clot is

doesn't matter how much clot there is if you're hypotensive for greater than 15 minutes then you fit in the massive category okay sub massive PE okay you have a normal blood pressure but your right ventricle is dysfunctional so

either by echo CT biomarkers such as BNP or troponin your EKG shows right heart strain basically your right ventricle shows some measure of duress but it has not totally decompensated to the point you're starting to get hypotensive and

I'll give you a pathophysiologic explanation in a couple slides low risk basically means that you have no hypotension no RV dysfunction no myocardial necrosis so you have clot in your pulmonary arteries absolutely but

your right ventricle is acting normal and you have no issues with hypotension that's 60% of pease that present to the hospital fortunately sub massive about 25% and massive five to ten percent okay why do we care about this categorization

is there any functionality this yes massive PE carries about a 25 to 65 percent mortality so it's a coin flip whether these patients are gonna live or die that's how severe this disease is sub massive PE you know these are the

patients that are compensated from a blood pressure standpoint but have RV dysfunction these patients have a three percent mortality or so in the most recent randomized now back in the late 90s and early 2000s

the mortality seemed to be higher on the order of 10% but I think we're settling around a 2 to 4 percent mortality for this group now these patients do have a higher rate of clinical deterioration than the low-risk group meaning they can

progress from the sub massive category to the massive category that's that 5% number there so this this group is a little bit that's why I said in yellow and the top group is in red low-risk patients anticoagulate them they'll be

fine so that was the eh-eh-eh in 2011 well the Europeans have to had to have their own version in 2014 and they said you guys you Americans are not doing this quite right so that's where they I'm sorry I can't put two pointers at

the same time that would be pretty cool but I'll start on this side if I can everybody over there see that all right so this intermediate group here is the same as the sub massive category I'm gonna walk you through this just because

it's you know we're more and more going towards the European Society guidelines so they break down this sub massive category into intermediate high and intermediate low and the reason they did that is they're saying that not all sub

massive pease are the same and that's probably true there's some some sub massives that are really not looking good and going towards massive and sub some some sub masters that are just rock solid stable and beside a little bit of

RV dysfunction they're probably gonna do just fine and just you know go towards the low-risk with a little bit of anticoagulation so what how do they break this down well both of them have this positive especi or pecci I'll show

you on the next slide what that is basically it's a pulmonary embolism severity index okay so you have to have that being abnormal or positive for you to fit in the intermediate category but then this is where it differentiates so

if you have an imaging test such as a CT or an echocardiogram and you have your laboratory biomarkers such as a troponin or BMP being elevated or abnormal then you fit into this intermediate high-risk category but if you have only one of

them or neither of them being positive in the intermediate low-risk category so what's the big deal why does that matter well but we don't really know frankly but what the European guidelines recommend

is if you're in this intermediate high category you should be watched because you have a risk of clinical deterioration and if you're going towards that they say consider reperfusion reperfusion could be

anything it could be systemic thrombolytics it could be catheter directed lytx or it could it could be surgery that's that's the way they put it if you're in the intermediate low-risk category you can be discharged

pretty early this is that pesi score and you can see why they tried to simplify it the s pesky because you have all of these factors and they're all assigned these points the more points you have the worse you are but let's focus on the

simplified pesky scale if you have a score of one or more of these then you're considered to have a 10% mortality in the next 30 days so that's these are what they thought were the highest impact issues in a patient

presenting with PE it doesn't tell you that just because you have a positive s peso you should intervene it just says that this is what may happen with these circumstance and we'll go through the first set just for a second here so age

greater than 80 years that's a that's an issue if you have cancer if you have heart failure or pulmonary disease a heart rate greater than 110 the systolic blood pressure less than 100 or an arterial oxygen saturation off of nasal

canula or supplemental oxygen less than 90% you get a point okay all right are we ready for the first question 65 year old man blood

so who are the most ideal candidates for fibroid embolization obviously I would say the most ideal candidates are patients that are symptomatic and I've told you already that 80% of black women

have fibroids but guess what only half of those will be so symptomatic that they would need to be even treated so just because fibroids exist don't mean that they need to actually be treated already so you

to actually have symptoms most patients that are symptomatic will again wait to getting treatment for like three and a half to five years but when they come we want to make sure that they're symptomatic and that they're not trying

to become pregnant and I know somebody in the audience has a question around that already so let's hold your high horses I'm coming to that how about patients that don't want to have surgery or just don't have time to

have surgery they don't have time for long recovery if you don't care if you have your uterus or not then I'm not so sure that you need to be pursuing a uterine sparing procedure okay and I'm gonna pause here to address one other

thing that it's a myth it is a myth that if you do not need to have children then you do not need your uterus I beg to differ and when we talk to women they are quite upset about this preposition that the uterus is only there for

baby-making purposes in fact there have been several studies now that have come out to say that women that have had early hysterectomy even with their ovaries in place are predisposed to coronary artery disease or

cardiovascular events we would like patients that are poor surgical candidates because if they can have surgery then they may be able to have surgery or patients that do not desire future fertility patients that have

already concerns about hysterectomy because of religious reasons or don't want to have hormonal therapy and I actually like patients that have have a have obesity because if we are able to do this procedure then they're spared

more complications related to surgery so the ideal patient then and this is a very important point said all three criteria would need to be fit that if you're a patient in order to be offered embolization number one

you have to have fibroids believe it or not you have to have symptoms that are related to fibroids and then you have to have some MRI that says that the location of where your fiber it is is causing that symptom and that these

fibroids are vascular let me explain okay and I'm going to skip this so I've been working with people for a long enough time and I've work of Julie for years I've worked with Diane and Anna and some other people for like ten years

and imagine if you're working with me for ten years you know that you're probably going to be able to do this procedure too like you're scrubbing right next to me eventually like you pick these things up what I get paid for

is not to do that and for the experienced nurses and techs that are in the room you know exactly what I'm talking about you're better than the doctors half of the time you really could do this procedure but what I get

paid for is to decide who does not even get to come on the table to get this procedure done so pay attention to this slide and these this criteria is being challenged every day and we're getting more and more data to say that this is

old information that we used to say if the uterus was like more than six months then you probably shouldn't have a uterine sparing procedure but we know that we do in embolization all the time in patients that have large fibroids

anyway but there's no data to actually give us that information most of the trials that we have and we have had a lot of them they have excluded patients where their individual fibroids were greater than 12 centimeters if you have

had an indeterminate and de metrio biopsy or you're having abnormal pap smear doing a uterine sparing procedure makes no sense so we use these imaging to really help us to determine which patients really

deserve to be treated so everybody can see that that image on the Left where it says submucosal refers to and I'm gonna try and come down so I can see these images here and you can see that there is a fibroid that is in

truck hava teri do you see that that round thing that is surrounded by the white fluid that is someone that has what we would call a type zero fibroid completely within the unit of course this is going to cause bleeding but

should this person have a uterine artery embolization or a hysterectomy Gail no this patient should have like hysteroscopic resection like a D&C and they would just scrape that thing out and then their symptoms would go away or

the patient on the right that has a normal appearing uterus and then this pedunculated gigantic thing that has bled into itself that is like a sub serosa fibroid of the extreme just hanging off on the outside now should

this patient have embolization no someone can tie a string right at that little connection and take that thing out so using our imaging to help us to decide which patients should be treated is very important or this patient who

came with Oh dr. Newsome I've been bleeding for 10 weeks in a row I have reversed cycles I have bulk I have bladder symptoms and yet they have that little dot that little black thing there that little dot

at the top that is the only place where there's a fibroid so this patient should not be a candidate for embolization either because yes they have symptoms and they have that little tiny daughter for fibra but that is not what's causing

those symptoms so it is important that we're not doing procedures on patients just because we can but because we're using our imaging and the patient's symptom to decide which patients are the best candidates for these procedures

study that was done was the perfect registry so all these studies have some name perfect the PE stands for pulmonary

embolism I don't know what the rest means but it's a registry of a hundred and one consecutive patients so these are patients that had what they termed at that time massive PE as well as sub massive PE it was seven sites and they

took all their data over three years so basically they said if you treated a patient with PE let us know send us all their info we're gonna put it in this one paper the therapy was all over the place for so patients with sub massive

or intermediate high risk PE they got catheter directed thrombolysis usually over 12 to 24 hours but again it was not specific it was whatever they did we want to know about it put it in one and sort of reported patients with

massive PE which are very different from those patients with intermediate high risk PE got mechanical fragmentation with some low-dose TPA and this was left open to whatever you were doing at your institution and then they looked at how

patients did overall and they looked at only survival to hospital discharge so they just want to know if patients like made it through that hospitalization overall they found that most patients were treated successfully so they didn't

die on the on the table and that they were able to get through there were six deaths for four mostly from the massive PE group and two from the sub massive and eighty nine point one percent had reduction in RV strain so that's one of

the risk factors or that's one of the goals endpoints that we look in in every study is RV strain did we improve their RV strain pre and post intervention and that can be measured either under an echo or on a CT scan one thing that we

don't know is by reducing that RV strain did we actually improve their life their quality of life or their overall survival and that's one some of the other studies mentioned 84% of these patients are almost 85 had a reduction

in their pulmonary artery pressure so as interventional radiologists and I believe interventional cardiologists also when we start our case we measure the pulmonary artery pressure we're really measuring the strain on the heart

as a result of the high pulmonary artery pressure so at the end of the case we want to know if we didn't even better and I always talk with our trainees and our team about the fact that once you do one of these cases you're really only

looking at the pressure you're not necessarily looking at what the picture looks like because sometimes the picture doesn't look very very good at the end of a PE lysis but the patients are doing much better one thing that's important

to notice is that there was a thirteen point one percent who had complications had complications that's a large number of patients so when you give patients thrombolysis they can have complications and many of them require blood

transfusions or have large hematomas or pseudo aneurysms and things that require further intervention the ultima study is another study this is a study looking at patients receiving unfractionated heparin so patients got just heparin and

other patients got Kathryn directive thrombolysis so this is the standard of care which is heparin versus TP a from a catheter this was a small group of patients only 59 patients and they were all patients who had acute PE with

an r v lv ratio greater than one so that's sort of night now the new standard the RVL v ratio should be less than one and that's basically just looking on a CT scanner and echo how big the RV is the left ventricle pumps all

the blood to the main to your body so that is much stronger than the than the right and it has a much larger size in on average and this is one of the methods that we use in all studies so what they looked at over time here is

these patients and how there are VL v ratio changed after they either received TPA or whether they got just the standard of care which is heparin and you'll see that there is an improvement in the patients who had a catheter

directed thrombolysis and overall they had better a change in their RV LV ratio so that's sort of the marker that we we have been using but again it still doesn't tell us do these patients live longer do they have better quality life

afterwards this Seattle to study is another study that was performed and this is actually a sort of a changing game-changing study at least for a catheter directed thrombolysis in the beginning this was a

industry-sponsored study it's May it was sponsored by the the makers of eCos catheters but it was what was nice about this study is that it was very well defined everyone had to do the same thing so if you're trying to study if

something works or not it's got to be consistent in this group they had massive patients and sub massive but they all had an RV LV ratio greater than 0.9 on CT every patient got unfractionated heparin or or lovenox low

molecular weight heparin and then they all received 24 milligrams of TPA that's the study everybody got the same thing and what you see here on this on the right is that the patients who had T who had catheter directed thrombolysis all

had a reduction in their RV LV ratio they all had a reduction in their mean systolic mean or systolic pulmonary artery pressure and they all had a reduction improvement in their Mead modified Miller index which is actually

a score of how much clot there is in the pulmonary arteries so that suggests that there's an improvement at least in the short term and these patients had reduced bleeding 13% vs. 10% is reduced it's not still

not great but these patients all got TPA so this is a summary slide from chest to in the chest guidelines in 2015 looking at the three studies I just mentioned to you so perfect Seattle - and Altima and it's basically again

showing you that there has been improvement in patients right ventricular strain as well as the patients mean systolic PA pressures but I will tell you even with this data we still don't know what the right answer

is because we don't know how this affects patients in the long term and how they're gonna do in their overall life so back to our patient to move on

so just a compliment what we everybody's talked about I think a great introduction for diagnosing PID the imaging techniques to evaluate it some of the Loney I want to talk about some of the above knee interventions no disclosures when it sort of jumped into

a little bit there's a 58 year old male who has a focal non-healing where the right heel now interestingly we when he was referred to me he was referred to for me for a woman that they kept emphasizing at the anterior end going

down the medial aspect of the heel so when I literally looked at that that was really a venous stasis wound so he has a mixed wound and everybody was jumping on that wound but his hour till wound was this this right heel rudra category-five

his risk factors again we talked about diabetes being a large one that in tandem with smoking I think are the biggest risk factors that I see most patient patients with wounds having just as we talked about earlier we I started

with a non-invasive you can see on the left side this is the abnormal side the I'm sorry the right leg is the abnormal the left leg is the normal side so you can see the triphasic waveforms the multiphasic waveforms on the left the

monophasic waveforms immediately at the right I don't typically do a lot of cross-sectional imaging I think a lot of information can be obtained just from the non-invasive just from this the first thing going through my head is he

has some sort of inflow disease with it that's iliac or common I'll typically follow within our child duplex to really localize the disease and carry out my treatment I think a quick comment on a little bit of clinicals so these

waveforms will correlate with your your Honourable pencil Doppler so one thing I always emphasize with our staff is when they do do those audible physical exams don't tell me whether there's simply a Doppler waveform or a Doppler pulse I

don't really care if there's not that means their leg would fall off what I care about is if monophasic was at least multiphasic that actually tells me a lot it tells me a lot afterwards if we gain back that multiphase the city but again

looking at this a couple of things I can tell he has disease high on the right says points we can either go PITA we can go antegrade with no contralateral in this case I'll be since he has hide he's used to the right go contralateral to

the left comment come on over so here's the angio I know NGOs are difficult Aaron when there's no background so just for reference I provided some of the anatomy so this is the right you know groin area

right femur so the right common from artery and SFA you have a downward down to the knee so here's the pop so if we look at this he has Multi multi multiple areas of disease I would say that patients that have above knee disease

that have wounds either have to level disease meaning you have iliac and fem-pop or they at least have to have to heal disease typically one level disease will really be clot against again another emphasis a lot of these patients

since they're not very mobile they're not very ambulatory this these patients often come with first a wound or rest pain so is this is a patient was that example anyway so what we see again is the multifocal occlusions asta knows

he's common femoral origin a common femoral artery sfa origin proximal segment we have a occlusion at the distal sfa so about right here past the air-duct iratus plus another occlusion at the mid pop to talk about just again

the tandem disease baloney he also has a posterior tibial occlusion we talked about the fact that angio some concept so even if I treat all of this above I have to go after that posterior tibial to get to that heel wound and complement

the perineal so ways to reach analyze you know the the biggest obstacle here is on to the the occlusions i want to mention some of the devices out there I'm not trying to get in detail but just to make it reader where you know there's

the baiance catheter from atronics essentially like a little metal drill it wobbles and tries to find the path of least resistance to get through the occlusion the cross or device from bard is a device that is essentially or what

I call is a frakking device they're examples they'll take a little peppermint they'll sort of tap away don't roll the hole peppermint so it's like a fracking device essentially it's a water jet

that's pulse hammering and then but but to be honest I think the most effective method is traditional wire work sorry about that there are multiple you know you're probably aware of just CTO wires multi weighted different gramm wires 12

gram 20 gram 30 gram wires I tend to start low and go high so I'll start with the 12 gram uses supporting micro catheter like a cxi micro catheter a trailblazer and a B cross so to look at here the sheath I've placed a sheet that

goes into the SFA I'm attacking the two occlusions first the what I used is the micro catheter about an 1/8 micro catheter when the supporting my catheters started with a trailblazer down into the crossing the first

occlusion here the first NGO just shows up confirmed that I'm still luminal right I want to state luminal once I've crossed that first I've now gone and attacked the second occlusion across that occlusion so once I've cross that

up confirm that I'm luminal and then the second question is what do you want to do with that there's gonna be a lot of discussions on whether you want Stan's direct me that can be hold hold on debate but I think a couple of things we

can agree we're crossing their courageous we're at the pop if we can minimize standing that region that be beneficial so for after ectomy couple of flavors there's the hawk device which

essentially has a little cutter asymmetrical cutter that allows you to actually shave that plaque and collect that plaque out there's also a horrible out there device that from CSI the dime back it's used to sort of really sort of

like a plaque modifier and softened down that plaque art so in this case I've used this the hawk device the hawk has a little bit of a of a bend in the proximal aspect of the catheter that lets you bias the the device to shape

the plaque so here what I've done you there you can see the the the the the teeth itself so you can tell we're lateral muta Liz or right or left is but it's very hard to see did some what's AP and posterior so usually

what I do is I hop left and right I turned the I about 45 degrees and now to hawk AP posterior I'm again just talking left to right so I can always see where the the the the AP ended so I can always tell without the the teeth

are angioplasty and then here once I'm done Joan nice caliber restored flow restored then we attacked the the common for most enosis and sfa stenosis again having that device be able to to an to direct

that device allows me to avoid sensing at the common femoral the the plaque is resolved from the common femoral I then turn it and then attack the the plaque on the lateral aspect again angioplasty restore flow into the common firm on the

proximal SFA so that was the there's the plaque that you can actually obtain from that Hawk so you're physically removing that that plaque so so that's you know that's the the restoration that flow just just you know I did attack the

posterior tibial I can cross that area I use the diamond back for that balloon did open it up second case is a woman

possible even though the you know strictures actually most likely are related to the malignant frequently in large centers like the Asura actually we see more benign strictures and malignant

strictures mainly because of the post-operative and perioperative complications so strictly speaking the incidence of reduced riches is actually flipped sometimes though we do actually have to help and some more patients now

particularly in the GI Sims I think in the ten last ten years GI now places metal stents almost routinely there's almost there are people still placing skinny in those things are two plastic calibers things

but the advent of retrievable removable metal stents has really changed and so now we will place dancing much frequently in that the wall stent is actually the pre derivative of the wall flex which is the Justin that can be

removed it's got a little barb that removes it and it's what they will do is retrograde put these up and then six weeks later or even up to nine months go in and retrieve it and pull them out completely so they certainly and the

number of build with stains placement in G and IR is reduced somewhat because how aggressive gr has become but certainly will place these and particularly patients who are in the palliative stages of care and although these

applications we've used in many other ways so your goal is to get the same team this just happens to be a patient with unresectable head of pancreas cancer you can see the obstruction in the distal CBD just below the cystic

duct there's non pacified area you can see on the calendar gram as well as the celiac artery gram you can see how the portal vein sensor strictures of his patients unresectable will go in there in place

that metal stent you first place your guide why follow that up with a stent that cross bridges from open to open and open this up and we use stands between eight and ten millimeters in diameter and nowadays even covering the

cystic duct is not such a big deal and nowadays cupboards things are probably more in favor now even though the data the data actually doesn't support covering over uncovered and the data for both is actually extremely marked be

similar and it's not compelling and because of the price difference I think visit again a probably a swing back to I'm not standing every CPD stains with covered stands but no question at least from operators point of view in my point

of view it makes whole wholehearted sense to allow the tumor no interest disease to grow through but yet the outcome is still not clear that it's a favorable and cost-effective to do covered stains entirely and we actually

will place up to three drains sometimes you have these complex cancer patients with multiple strictures where almost all the segments are excluding in a extremely sick or they need their bilirubin's to come down for four to be

eligible for cut medical oncology chemotherapy and this is the selling of metastatic colorectal cancer and so that will put three up to three tubes in the right lobe before will give up and say that there's not much more decompression

we can achieve so four tiers is that probably the maximum will place in for multiple site so like I said you know malignant brutally strictures and this data and I'm not going to because it's sort of a moving target

when Gore came with the first covered stand purely because of the fabric that they have gore-tex like what's under jacket and clothing and was interesting it's one of the most improbable fabrics and the reasons why Bill Lewis stands

accrued is not so much that it's overgrowth of tumor but the in growth of bio and in growth of bacteria actually will cause a non-covered stain suit include earlier so the advent of gore and making a stent that made a big

difference and it's covered same it does to change quickly the ease at which patients could be stent in the new system so when they came on the market was really helpful and there's just example of how you can go from occlusion

all the way to having natural passage about now back into the small bar and the utility and the importance of bile salts power fluid in your GI tract is critical for absorption in almost all your metabolic

function so having this drain out externally is really not advisable so getting a natural pathway flow of bio into the GI system is extremely important but I believe strictures and

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