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Transcript

approach to pulmonary embolism.

This is a guy 22-year-old who has ARVC, which is arrhythmogenic right ventricular cardiomyopathy. Which is a bad condition whereby you get fibrosis and fat infiltration of your right ventricle, and essentially it becomes this very flabby,

very enlarged, very thrombogenic as well as very arrhythmogenic right ventricle. So this guy he was systemically unwell, but he presented with an acute decompensation where he got ventricular tarchycardia storm. And that's where you just are in V tacky constantly. He had an

ASCDA and this was shocking him 20 times a day when he presented. Very hypoxic guy as well, he was on Rumer/g he was done at 88% really was quite difficult to improve. Lucky or unlucky as well as all that he developed massive hemoptysis. This was so bad that he needed intubation to prevent a spill over

from presumably it was a right sided hemoptysis based on his chest X ray. As soon as he got intubated of course the usual thing that happened is, he decompensated further from a cardio respiratory point of view. And that's where we got urgently consulted.

So he was rushed for a CT, you can see he'd already been interbated at this time. His right ventricle looks terrible, his right artrium was a large volume thrombus or venous and in his lumbar and segmental both sides,

but predominantly on the right side he had a moderate volume thrombus there. So we restratified this gentleman as a massive presentation given the fact that he was hemodynamically compromised, and previously arrested with [UNKNOWN].

And then came up with our decision making algorithm. So this is a gentleman who was hemoptysizing massive hemoptysis requiring intubation, but the gentleman who had a large volume thrombosis in his lungs.

Eventually a decision was reached between everyone that he could not be lysed so we proceeded with mechanical thrombectomy. Obviously there are a couple of different options you can use there I felt that in my hands using a large caliber device such as the flowtreiver the Inari or the angio vac and a guy who is having recurrent arrhythmias would not be terrifically safe.

I didn't feel I'd be able to get it around to get the thrombus without him arresting again, so I decided to use a low profile device. So we came in from the neck as we do most of our interventions in pulmonary arteries from the neck. Came round you can see this occlusive thrombus here within the [INAUDIBLE] lumbar

artery, and then I used a device called cleaner. Which is rotation sinusoidal 035, 344 depending on which one you use. We use the 7 French device you can see here on the echo this is in the right main PA. Echo is very handy for monitoring of this main PA interventions so

you really get live real time updates that can be pretty helpful, particularly for doing aspirational thrombectomy that can tell you what your end point is and where you're gonna stop. So chopped up some of the clot with that you here you can see it on the angio view at it working in the area of [INAUDIBLE] thrombus. And then aspirated the thrombus that we had hopefully broken up

using the indigo device from panumbra. We use the cath six here for some reason we'd run out of catheters at the time, otherwise it would have put that. So this was 6 French aspiration device and we got out a descent amount of thrombus over the course of about an hour, or so he began

to stabilize he was never terrific to be honest but he stabilized somewhat. So he wasn't having anymore arrhythmias, no further shocks to his AACD and we were able to bring him up stairs. So success I think it's difficult to quantify how much good we actually

did, because two days later after he had some neurologic signs of improvement he proceeded to have ECMO. And then he went on to have a heart transplant for his AACD 30 days later and actually this is about a year ago, he's been doing very well, we pulled out the filter,

we placed at the time nine months and he's been doing great. So I think overall the procedural success, certainly a patient success is debatable to how much we contributed to his overall success.

And those are two of the cases. Thanks.

access reowww lytic thrombectomy or the angio jet device which is the most frequently used device for this what it does is basic disrupts the clot by shooting out TPA

embeds it into the clot and then you suck it up using suction thrombectomy using the venturi effect and you aspirate some of the clot and you can see that here that's a picture from I think the angio jet website the benefit

is that it can be you can use it without TPA and just use the suction thrombectomy mode with heparinized saline and that can be helpful to help break up some clot the drawbacks is that it has a black box warning from the FDA

so we do this every once in a while in the right patient but this is definitely not recommended by the company or anyone for that matter but it does work in some cases and the main reason is that the the vibrations caused by the device can

cause significant bradycardia in addition to the bradycardia that you get from red blood cell really lysis that you get with these devices so you actually couldn't cause arrhythmia on top of bradycardia which sounds like a

bad a bad combination and these patients can get hemodynamic collapse and die right on the table just cuz you turned on the device so that being said we've all I think done it once or twice I've seen I've only done it once and I never

do it again because a patient coded one of my colleagues did it on a patient because the patient was already coding said well what's the harm and that patient survived they did better actually because we were able to break

up the clot so I will say that if you do it and the patient doesn't do well you really don't have a leg to stand on because right on the cover of the packaging it says do not use in the pulmonary arteries aspiration

people were thinking about the covered

portion actually actually would be occlusive in that paddock veins a lot of people are concerned about that this could be kind of like a but carry you're gonna actually occlude flow in the paddy vein caused thromboses that didn't pan

out at least clinically okay it didn't pan out and that's another advantage of actually accessing very close to the paddock vein IVC junction that's where the biggest vein is so you don't get a lot of occlusive problems okay but

usually clinically it does not pan out so the bigger the hepatic vein the more likely you have a lot of room around your your graft you won't be occlusive to the paddock vein that's more important for for transplants than other

than others I told you it's rare this is actually a very rare case of such that where you actually have a segmental segmental kind of but carry after a tips okay and you know this is actually from a form of venous outflow from the ematic

vein this is a perfusion defect typical it's a wedge right typical perfusion defect in the liver that's how you death so you know this is vascular this is a perfusion problem but you've got hepatic artery readout artery the red arrows

running into the segments and you have portal vein running into the segments so what's the problem it's actually a paddock vein occlusion okay by the stents subclinical no no clinical complaints you let it be

in the patients usually recover okay treat the patients and not the images okay on the other side if you put their tips too deep sometimes you actually get thromboses of the portal vein branch

again you get a call from hepatology you've got portal vein thrombosis is the patient doing okay yes treat the patient and not the images they usually resolve this it's not not a big problem another technical problem

I'm gonna focus mostly on technical for you guys this is a but key area okay and the but carry especially in the acute stage the liver is not like a cirrhotic liver is big liver is actually engorged okay so it's very large usually

your needle is too short to even reach the portal vein okay that's a big problem okay because your access needle is too short for a very large engorged the portal vein so this is as deep as it

goes do I have a see that that do you see that needle tip that's as deep as the needle tip goes okay the portal vein is a good distance away okay luckily this is a co2 porta gram luckily I'm actually in a small branch right

there I just hit it on you know and on this is not the there's not a needle tract this is just luckily hitting it a little branch and on so I'm actually accessing the portal vein and I can do a co2 porta gram here okay

typical inexperienced person would say you know this looks good I'm lucky I'm in a branch but it's a nice smooth curve I'll just pass a wire down and I'll balloon it and I'll put a stent in it's a nice curve and you know so it's my

lucky day I don't need to extend my needle or get a bigger longer needle to reach the portal vein here's the problem with this and this is exactly what this is exactly what this is they pass a wire and it looks beautiful just put a stent

and go home okay here's the problem this is actually the small branch access sites this is actually where you really need to access world vane but your needle is not long enough okay

what we found out is that if you are in a small in a small portal vein no matter how much you balloon it it will come down again and it will be narrow so believe it or not if you go sideways in a portal vein and rip it open with a

balloon it will stay open but if you go down of small portal vein and balloon it open it will always contract down okay so you cannot do a tips simply by ballooning and putting a stent in in this case okay what we do is we actually

denude the vein itself we actually rip it off okay and make it a raw parenchyma and we do that with a Tortola device we literally rip off the paddock the paddock portal sorry the portal vein endothelium and media and adventitia rip

it off make it completely raw as if it's an access as if it's a liver brain coma which is which it is now and then we then we balloon dilates okay rip it off denude it angioplasty it's okay and then put the stent and see that aggression

despite all that aggression of ripping it off it still has an hour kind of an hourglass shape to the to the tips okay that little constraint there that's the hepatic venous access sites this is the parenchymal tract to see nice and open

with a balloon but the but the actual vein that we've been through despite our aggression in actually ripping it off it's still narrowed down but this is as good as it gets okay

now other causes this is a little bit different different scenario here but it's not always just as simple as all

there's leaky valves in the gonadal vein that are causing these symptoms this is 38 year old Lafleur extremity swelling presented to our vein clinic has evolved our varicosities once you start to discuss other symptoms she does have

pelvic pain happiness so we're concerned about about pelvic congestion and I'll mention here that if I hear someone with exactly the classic symptoms I won't necessarily get a CT scan or an MRI because again that'll give me secondary

evidence and it won't tell me whether the veins are actually incompetent or not and so you know I have a discussion with the patient and if they are deathly afraid of having a procedure and don't want to have a catheter that goes

through the heart to evaluate veins then we get cross-sectional imaging and we'll look for secondary evidence if we have the secondary evidence then sometimes those patients feel more comfortable going through a procedure some patients

on the other hand will say well if it's not really gonna tell me whether the veins incompetent or not why don't we just do the vena Graham and we'll get the the definite answer whether there's incompetence or not and you'll be able

to treat it at the same time so in this case we did get imaging she wanted to take a look and it was you know shame on me because it's it's a good thing we did because this is not the typical case for pelvic venous congestion what we found

is evidence of mather nur and so mather nur is compression of the left common iliac vein by the right common iliac artery and what that can do is cause back up of pressure you'll see her huge verax here and here for you guys

huge verax in that same spot and so this lady has symptoms of pelvic venous congestion but it's not because of valvular incompetence it's because of venous outflow obstruction so Mather 'nor like I mentioned is compression of

that left common iliac vein from the right common iliac artery as shown here and if you remember on the cartoon slide for pelvic congestion I'm showing a dilated gonna delve a non the left here but in this case we have obstruction of

the common iliac vein that's causing back up of pressure the blood wants to sort of decompress itself or flow elsewhere and so it backed up into the internal iliac veins and are causing her symptoms along with her of all of our

varicosities and just a slide describing everything i just said so i don't think we have to reiterate that the treatments could you go back one on that I think I did skip over that treatments from a thern er really are also endovascular

it's really basically treating that that compression portion and decompressing the the pelvic system and so here's our vena Graham you can see that huge verax down at the bottom and an occluded iliac vein so classic Mather nur but causing

that pelvic varicosity and the pelvic congestion see huge pelvic laterals in pelvic varicosities once we were able to catheterize through and stent you see no more varicosity because it doesn't have to flow that way it flows through the

way that that it was intended through the iliac vein once it's open she came back to clinic a week later significant improvement in symptoms did not treat any of the gonadal veins this was just a venous obstruction causing the increased

pressure and symptoms of pelvic vein congestion how good how good are we at

I like to talk about brain infarc after Castro its of its year very symbolic a shoe and my name is first name is a shorter and probably you cannot remember my first name but probably you can remember my email address and join ovation very easy 40 years old man presenting with hematemesis and those coffee shows is aphasia verax and gastric barracks and how can i use arrow arrow on the monitor no point around yes so so you can see the red that red that just a beside the endoscopy image recent bleeding at the gastric barracks

so the breathing focus is gastric paddocks and that is a page you're very X and it is can shows it's a page of Eric's gastric barracks and chronic poor vein thrombosis with heaviness transformation of poor vein there is a spline or inertia but there is no gas drawer in urgent I'm sorry tough fast fast playing anyway bleeding focus is gastric barracks but in our hospital we don't have expert endoscopist

for endoscopy crew injections or endoscopic reinjection is not an option in our Hospital and I thought tips may be very very difficult because of chronic Peruvian thrombosis professors carucha tri-tips in this patient oh he is very busy and there is a no gas Torino Shanta so PRT o is not an option so we decided to do percutaneous there is your embolization under under I mean there are many ways to approach it

but under urgent settings you do what you can do best quickly oh no that's right yes and and this patience main program is not patent cameras transformation so percutaneous transit party approach may have some problem and we also do transit planning approach and this kind of patient has a splenomegaly and splenic pain is big enough to be punctured by ultrasonography and i'm a tips beginner so I don't like tips in this difficult

case so transplanting punch was performed by ultrasound guidance and you can see Carolus transformation of main pervane and splenorenal shunt and gastric varices left gastric we know officios Castries bezier varices micro catheter was advanced and in geography was performed you can see a Terrell ID the vascular structure so we commonly use glue from be brown company and amputee cyanoacrylate MBC is mixed with Italy

powder at a time I mixed 1 to 8 ratio so it's a very thin very thin below 11% igloo so after injection of a 1cc of glue mixture you can see some glue in the barracks but some glue in the promontory Audrey from Maneri embolism and angiography shows already draw barracks and you can also see a subtraction artifact white why did you want to be that distal

why did you go all the way up to do the glue instead of starting lower i usually in in these procedures i want to advance the microcatheter into the paddocks itself and there are multiple collateral channels so if i in inject glue at the proximal portion some channels can be occluded about some channels can be patent so complete embolization of verax cannot be achieved and so there are multiple paths first structures so multiple injection of glue is needed

anyway at this image you can see rigid your barracks and subtraction artifacting in the promenade already and probably renal artery or pyramid entry already so it means from one area but it demands is to Mogambo region patient began to complain of headache but american ir most american IRS care the patient but Korean IR care the procedure serve so we continue we kept the procedure what's a little headache right to keep you from completing your

procedure and I performed Lippitt eight below embolization again and again so I used 3 micro catheters final angel officio is a complete embolization of case repair ax patients kept complaining of headache so after the procedure we sent at a patient to the city room and CT scan shows multiple tiny high attenuated and others in the brain those are not calcification rapado so it means systemic um embolization Oh bleep I adore mixtures

of primitive brain in park and patient just started to complain of blindness one day after diffusion-weighted images shows multiple car brain in park so how come this happen unfortunately I didn't know that Porter from Manila penis anastomosis at the time one article said gastric barracks is a connectivity read from an airy being by a bronchial venous system and it's prevalence is up to 30 percent so normally blood flow blood in the barracks drains into the edge a

ghost vein or other systemic collateral veins and then drain into SVC right heart and promontory artery so from what embolism may have fun and but in most cases in there it seldom cause significant cranker problem but in this case barracks is a connectivity the promontory being fired a bronchial vein and then glue mixture can drain into the rapture heart so glue training to aorta and system already causing brain in fog or systemic embolism so let respectively

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

of the simulation and mentis simulator that we purchased that our system and purchased it's used in conjunction with

the cardiologists and first second third year cardiac fellows interventional fellows who also have the opportunity to practice on this but what I really liked about this and what really surprised me is how real it

is for learners and for our texts that come in our technologists using this piece to move the C arm to move it left to move it right injecting contrast which is actually air but you know we want to say it's contrast I'm moving the

table understanding how to pan the table how to move the CRM there's a lot of different functions that they can use collimation magnification so this board this panel is pretty much what they're going to do on a daily basis so this is

extraordinary and the picture next to it shows us some 3d dimension three-dimensional pictures of the coronary arteries laid out in different projections so depending on how you move your C arm you'll be able to see the

different angles of your coronary arteries again this is live real-time simulation 3d dimensions so we don't have to actually inject the contrast to visualize our coronary arteries in our a Horta there's a function button that you

can push and it automatically displays the three dimensions so it makes it easier for us to identify those arteries without having to inject and show the different views so it's fascinating in more pictures that showing doctor Lee

came who came to Phoenix Banner University Phoenix to help demonstrate so this is our first week after we've introduced the mentis to our learners and had them play with some of the functions again following up with dr.

Lee's visit he's the one that questioned our staff our learners and reiterated what Michael and I have taught in the first week so basically just understanding and reiterating everything that we went through and having our

learners hear it again from the physician what does he want how does he expect his staff to participate in how do his how does he expect his so what are the expectations of our learners so he was really forward he

asked them great questions they answer them because we taught them but we also showed that he also was able to show them some techniques that they as physicians would like the learners to know right so um he is the clinical

expert obviously so it was really nice to see them interacting together and answering questions again just another photograph of one of our learners using the mentis and showing the actual x-ray view on the left and showing the 3d

dimension on the right these are this is our photograph so we took these pictures during our last week of our programs so this is our final wrap-up putting it all together so we basically took them to the lab we we borrowed one of the labs

we asked our operational leaders if we could borrow one of the labs they weren't using that day and we came in and we set it all up we wanted to make sure they knew how to open a tray how does that how to set the table how to

set the back table how to prep the table how to get their power injections their med rads or their assists put together so we really went from A to Z during this wrap up final simulation study so our learners gound and glove they put on

their PPE and we did have the mentis underneath the drape so they were able to drape as if it was a real patient and also manipulating those wires so we had our cardiology fellow interventional fellow first I think it was first year

in second year who came to assist they were gracious enough to come in and help us assist that piece while Michael and I could focus on the learners helping them navigate through that lab calling out for supplies calling out for wires

calling out for stents calling out for balloons so it was pretty realistic and I think I think our learners really enjoyed that this is just another view of our table being set up one of our learners

scrubbed in she was an RN and she was learning kind of moved the table again you don't really get to do that in real life but in simulation all is game so they got to play and here's an image of our cardiology fellow it's not playing

so what it shows is the simulation of the angio angiogram of the coronary arteries so while we inject the contrast you can see the arteries filling in that simulation unfortunately we can't seem to get it to play again more pictures of

me teaching them how to move the table and the position that they needed to be in so and so we also wanted to make it

from our acute to chronic again just to recap this patient had what was

confirmed categorized as intermediate high risk PE for many of the reasons that you can see here so again here's their scan showing that there's thrombus in the left and right pulmonary arteries here's an echo that showed that the

patient had right ventricular strain and that had an enlarged right ventricle so this patient got a pulmonary artery Graham you can see here there's thrombus you basically don't see contrast going past the main pulmonary artery on the

right or the left sorry I didn't have the DSA images so we check we put a pulmonary artery catheter we do some initial runs and get pressures and then afterwards we put wires into the main pulmonary arteries ideally we try to go

down into the lower lobe so you get the most bang for your buck and have throw-up I have TPA infusing in the area that has the most rhombus and then we in this case placed eCos catheters and you can tell whether catheters Annie Coast

catheter not because of the little hash marks one thing that's important to notice is that the hash marks don't go all the way to the end the first time I need to Nicko's catheter I didn't know that and I was like I think the wire is

too short that's inside of it but it actually is short by a few centimeters the patient came back 24 hours later you can already see that there's an improved profusion in the left lung all the way distally and then in the right lung you

can also see improved perfusion so they're still thrombus they're in the right lower lobe again we're not going for a perfect picture what we're going for is the patient to be better and their pulmonary and the right

ventricular pressures to be improved if the pressure is reduced about 20% I think most interventional radiologists will say that that's a successful procedure but more importantly what I'd like to

see is that the patient is no longer on pressors they're no longer requiring a high amount of oxygen they can be extubated they say that they don't have any more chest pain they're able to talk better all of those clinical factors

that we sort of sometimes don't think about those are signs that the patient is doing well and that maybe that's not worth the risk of continuing giving him the TPA so this is a follow-up scan on this patient showing that pretty much

all the thrombus is gone so what happens

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

us off so here's the case from 2011 52 year old woman with asymptomatic PE who gets transferred for an outside hospital to the medical intensive care unit on a mid Saturday I'm at the humorous bit the University of Maryland at this point one

of my partners over there where is she right back there over there the two of them are they are hot hot hot stars right there in the back therapeutic Lee anticoagulated consulted the NICU attending calls me directly

the woman is hypoxic her blood pressure is low the something happens in PowerPoint and then we restart again this has taken its own independent control right now that's alright my back all right I get

to press the green button here we go green button has been pressed no action green button again there we go alright so her o2 saturation is low she's hypotensive she gets a lot of fluid her o2 saturation improves and supposedly

she was able to talk comfortably and they watch her so the question was maybe she should get some intravenous TPA that actually is the thing on the bottle versus in an ir calf direct intervention or heparin at 8 so they continue with

mchugh supports not looking bad at 8:30 at night some hours later I get a new call she's hypotensive now newly so despite therapy she's working harder to breathe an echo has been done it took hours to get the result her right side

of her heart is struggling which is the thing that happens with big pease a bad sign we can look at blood levels of troponin x' and things as well and she's now in IR by 8:30 at night so we move quickly at this point in the room she's

breathing comfortably on 3 to 4 liters of nasal cannula and she's able to talk to me and lie flat in the procedure suite this is a vena cava grant so I've cued us to some of the findings which is the flow is up the vena cava and

backwards into the apat of aim it's going up and it's coming back down so you can it you can flood the vena cable with so much contrast that it's going to spill back because you just overfill it but this is not that injection this is

hand injection ok so that means that something's happening downstream and that's the right heart not able to handle the load of contrast not a good sign actually 10 for 20 I made that number up

because I couldn't remember but I can tell you it wasn't over injected so the mean pulmonary pressure is 55 high low normal okay we got a we got a high sign over there from UVA basketball go so so at this point I'm anxious because she's

anxious and visibly so so we start to hustle to get into the pulmonary arteries and she's starting to do less well very quickly this isn't going to be mechanical thrombectomy I give a race 1/2 systemic bolus that's

a that's actually a high dose of TPA immediately because I'm now hoping that systemic therapy is gonna work as she's decompensating we are preparing to do thrombectomy pressors are being started I give more

TPA which is an indication of being worried she's now intubated CPR particular fibrillation she shock we code her for 40 minutes and she dies in ion so we have the pulmonary Catherine and we haven't started the therapy even

so the question of course is what did we miss beforehand and this is before her okay what sign should have happened sooner yes she was hypercoagulable plus I think a very would this have made a difference it's not so clear even

retrospect did we just pour fluids into her which will keep a blood pressure up and moving on that Starling heart curve that says you heart muscle will continue to work and then you fall off that cliff and would it been done differently on a

Saturday all those kinds of you know on

another device that's new in the market

is the inari device it is a combi combination of suction thrombectomy and mechanical thrombectomy and it you can see it looks like three Amplatz or plugs on a catheter but that blue catheter is actually a very nice suction system as

well so you can go beyond the clot pull it in and then suck it into the catheter this is very useful because you can pull clot out without giving any TPA and you have a lot less blood loss so if you can take the clot out with a lot less blood

loss I think you can out patients again the benefit is that there's no thrombolytic and the patients have less bleeding drawbacks like many of these devices is there's really no studies to prove that they work we can prove that

they can remove clot from the patient's body but that we don't know that that actually helps in the long run so what we really want to know in all the studies which we're actually going to show three of the main studies is

whether this actually helps patients life in the long term do they does it improve their mortality so the first

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

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

plan as well so I wanted to talk a

little bit about imaging I know with our residents and fellows and radiology that's all we do is talk about the imaging and then when go on to IR we talked to them about the intervention but I think it's important

for everyone in this room to see more imaging and see what we're looking at because it's very important for us all to be doing on the same page whether you're a nurse a technologist a physician or anybody else in the room

we're all taking care of that patient and the more information we all have the better it is for that patient so quick primer on a PE imaging so this is a coned in view of a CT pulmonary angiogram so yeah sometimes you'll see

CTS that are that are set for a pulmonary artery's and you'll see some that are timed for the aorta but if the pulmonary arteries are well pacified you're gonna see thrombus so I have two arrows there showing you thrombus that's

sort of blocking the main pulmonary arteries on the left and right side on the patient's left so the one with the arrow that is a sort of very classic appearance of an intro luminal thrombus you can see a little rim of contrast

surrounding it and it's usually at branch points and it's centered in the vessel the one on the right with the arrow head is really at a big branch point so that's where the right lower lobe segmental branches are coming off

and you can see there's just a big amount of thrombus there you can see distal infarct so if you're looking in the long windows you'll see that there's this kind of it's called a mosaic perfusion but it also what kind of looks

like a cobweb and that's actually pulmonary infarct and maybe some blood there which actually will change what we're gonna do because in those cases freaken we will not perform PE thrombolysis it's also important to note

that acute and chronic PE which we're here to talk about today may look very similar on a CT scan and they have completely different treatment methods so here's a sagittal view from that same patient you can see the CT scan so

between the arrow heads is with the tram track appearance so you'll see that there's thrombus the grey stuff in the middle and you'll see the white contrasts surrounding it and kind of like a tram track and that's very

classic for acute PE and then of course where the big arrow is is just the big thrombus sitting there here's another view of a coronal this is actually on a young woman which I think we show some images on but you can see cannonball

looking thrombus in the main pulmonary arteries very classic variants for acute PE and then this is that same patient in a sagittal view again showing you in the left pulmonary kind of those big cannon balls of

thrombus here's some examples from the literature showing you the same thing when you're looking at an acute PE it's right centered on all the image all the way in the left if the classic thrombus is centered right in the middle of the

vessel you can usually see a rim of normal contrast around it and you can see on a sagittal or coronal view kind of like a thin strip of floating thrombus so the main therapies for acute

original classification of PE is important to know because it man it helps dictate treatment so it used to be classified as massive which is about 5% of PE patients these are the ones that

we all know how to treat they're usually coding essentially when they show up to the ER or to the angio suite or in the ICU they have a 58% ninety day mortality rate so these patients are doing very poorly they're in hemodynamic collapse

which is the diagnostic factor there that sort of makes that diagnosis because of cardiogenic shock sub massive PE is the biggest group that we'll talk about last I'm sorry the most important group we'll talk about last so

minor PE are about 55% of PE patients those are the ones that show to the ER that just don't feel right and they turns out that they have PE so it was really not even anyone's differential diagnosis and most of these patients do

just fine with outpatient anticoagulation monitoring and monitoring so the main group that matters in that most of the talks about PE are about are the sub massive group which is about 40% of patients and these

are the ones that show up with a moderate amount of clot and some right ventricular strain these are the patients who are able to tolerate their PE but they're not doing very well so they come in with shortness of breath

some chest pain and although they're not in hemodynamic collapse they are the ones who require inpatient monitoring or their good it goes to an ICU and that's really the patients that we worry about those are the ones that we're going to

do an intervention on or systemic TPA so that was the sort of the old way of classifying PE and this is the new way of classifying PE so this is the Europeans Society of Cardiology they had a

consensus in 2014 talking about PE and what we look at now and the way we stratify these are high risk PE intermediate which is intermediate high and intermediate low and then low risk PE so this is

important because it in fact it utilizes patients actual biomarkers imaging as well as their clinical symptoms all in one and so what we look at if you look at a patient with high risk PE they have to be in shock or hypotension that is

one factor that has to be there and actually everything else doesn't matter but the things that we look at are the PE severity index or the PES e score if you google PES e PE SI it's basically a bunch of things it asks for the

patient's age whether they have cancer what their heart rate is if what they're owed to sat and on what oxygen content they're on and it gives you a score and that classifies it in 1 through 5 and basically 5 is really bad which means

that you have a low or you have a higher mortality as an outpatient and 1 is really low some things like cancer give you a lot of points so that sort of pushes it over to automatically kind of 2 3 then you look at the signs of our V

dysfunction and really with PE that's really the thing that that kills you is your right ventricular dysfunction and if your right heart fails then your left heart fails and then you die and so that's really where the issue is

and then the cardiac laboratory biomarkers are what will sort of give you a blood test that you can figure out and see if that patient is going to do poorly so high risk PE shock or hypotension

low risk Pease the other end where you really don't have any of those things but you do have a PE diagnosed either usually on a CT scan but it could be on an echo as well intermediate high and intermediate low is where we all spend

all the time talking about that's what we kind of do all the studies on is really the intermediate high and low groups and what we should do for them and sort of how we can affect their lives but the main point here that I

want you to see is that they don't have shock or hypotension but they do have positive right ventricular strain either on an echo or a CT scan and they have positive biomarkers if you have positive biomarkers and imaging then you have

intermediate high risk PE and those are the patients who may benefit from some sort of intervention or some sort of further ICU monitoring and anticoagulation so I'm gonna just

next is me talking about Egypt and Ethiopia and how I are how IRS practice in Egypt and Ethiopia and I think feather and Musti is gonna talk a little bit about Ethiopia as well he's got a

lot of experience about in about Ethiopia I chose these two countries to show you the kind of the the the the difference between different countries with within Africa Egypt is the 20th economy worldwide by GDP third largest

economy in Africa by some estimates the largest economy in Africa it's about a hundred million people about a little-little and about thirty percent of the population in the u.s. 15 florist's population worldwide and has

about a little over a hundred ir's right now 15 years ago they had less than ten IRS and fifteen years ago they had maybe two to three IRS at a hundred percent nowadays they're exceeding a hundred IRS so tremendous gross in the last 15 years

in the other hand Ethiopia is a very similar sized country but they only have three to five IRS that are not a hundred percent IRS and are still many of them are under training so there are major differences between countries within

within Africa countries that still need a lot of help and a lot of growth and countries that are like ten fifteen years ahead as far as as far as intervention ready intervention radiology

most of the practice in Ethiopia are basic biopsies drainages and vascular access but there is new workshops with with embolization as well as well as well as vascular access in Egypt the the ir practice is heavily into

interventional oncology and cancer that's the bulk that's the bulk of their of their practices you also get very strong neuro intervention radiology and that's mostly most of these are French trained and not

American trains so they're the neuro IRS in Egypt or heavily French and Belgian trains with with french-speaking influence but the bulk of the body iron that's not neuro is mostly cancer and it involves y9e tastes ablations high-end

ablations there's no cryoablation in Egypt there is high-end like like a nano knife reverse electric race electroporation in Egypt as well but there is no cryo you also get a specialty embolization such as fibroids

prostate and embroiders are big in Egypt they're growing very very rapidly especially prostates hemorrhoids and fibroids is an older one but it's still there's still a lot of growth for fibroid embolization zyou FES in Egypt

there's some portal portal intervention there's a lot of need for that but not a lot of IRS are actually doing portal intervention and then there's nonvascular such as billary gu there's also vascular access a lot of

the vascular access is actually done by nephrology and is not done by not not done by r is done by some high RS varicose veins done by vascular surgery and done by IRS as an outpatient there's a lot of visceral angiography as well

renal and transplants stuff so it's pretty high ends they do not do P ad very few IR s and maybe probably two IR s in the country that actually do P ad the the rest of the P ad is actually endovascular PA DS done by vascular

surgery a Horta is done all by vascular surgery and cardiothoracic surgery it's not done it's not done by IR IR s are asked just to help with embolization sometimes help with trying to get a catheter in a certain area but it's

really run by by vascular surgeons but but most more or less it's it's the whole gamut and I'm going to give you a little example of how things are different that when it comes to a Kannamma 'kz there's no dialysis work

they don't do Pfister grams they don't do D clots the reason for that is the vascular surgeons are actually very good at establishing fishless and they usually don't have a

lot of problems with it sometimes if the fistula is from Beau's door narrowed it's surgically revised they do a surgical thrombectomy because it's a lot cheaper it's a lot cheaper than balloons sheaths and and trying to and try a TPA

is very expensive it's a lot cheaper for a surgeon to just clean it out surgically and resuture it there's no there's no inventory there are no expensive consumables so we don't see dialysis as far as fistula or dialysis

conduits at all in Egypt and that's usually a trend in developed in developed countries next we'll talk

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

higher procedures that get done in the country so they are from being basics such as being para sentences and in some

centers being quite complex in Euro work and there are centers where these none of all those that IR procedures being available so it's a very unequal distribution of provision of IR services and like I mentioned earlier on vascular

surgeons and cardiologists have basically taken over the peripheral vascular work and iogic work and other known neuro speciality such as bid early interventions for example saying that these two surgeons who are in some

remote centers who are doing their own provision as biliary basic interventions there is one neuro surgeon who went and had neuro imaging and then your interventional training who is now hundred percent doing a mural

intervention so as far as procedures go my day can be in diagnostic work and you might be dreaming you doing a paracentesis the next thing you might be doing some some I our basic IR and on the same day you might be doing a set

procedure so quite varied but not available in all centers as one would want as fine stuff goes the technology

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

quick I did want to mention t-carr briefly and try to get you guys closer to back on time this is a hybrid procedure this is combining the surgical procedure we talked about first and carotid stenting it takes combined

carotid exposure at the base of the clavicle or just above the clavicle and reverses blood flow just like we talked about but tastes slightly different technique or approach to doing this and then you put the stent in from a drug

carotid access here's the components of the device right up by the neck there is where the incision is made just above the clavicle and you have this sheet that's about eight French in size that only goes in about us to 2 cm or 1 and a

half cm overall into the vessel and then that sheath is sutured to the the chest wall and then it's got a side arm that goes what's labeled number six here is this flow reversal urn enroute neuroprotection kit it reverses the

blood flow and then you get a femoral sheath in the vein right in the common femoral vein and you reverse the blood flow so this is a case a picture from our institution up on the right is the patient's neck and that's the carotid

exposure and the initial sheath is in place so the sidearm of that sheath is the enroute protection system which is going up up at the top of the image there we're gonna back bleed that let that sidearm of that sheath continue to

bleed up to the very top and then connect that to the common femoral venous sheet that we have in place there's a stepwise of that and then ultimately what we see at the end of the procedure is that filter inside that

little canister can be interrogated after and you can see the debris this is in the box D here on the bottom left the debris that we captured during the flow reversal and this is a what we call a passive and then active flow reversal

system so once the system is in place the direct exposure carotid sheath in place the flow controller and AV shunt in place you see the direction of blood flow so now all that blood flow in that common carotid artery is going reverse

direction and so when you place a sheath or wire and and ultimately through that sheath up by the carotid artery there's no risk for distal embolization because everything is flowing in Reverse here's a couple

case examples ferns from our institution this is a patient who had a symptomatic critical greater than 90% stenosis has tandems to nose he's so one proximal at the origin and one a little bit more distal we you can see the little

retractors down at the base of the image there in the sheath that's essentially the extent of the sheath from the bottom of that image into the vessel only about a cm or two post angioplasty instant patient tolerated that quite well here's

another 71 year-old asymptomatic patient greater than 90% stenosis pretty calcified lesion a little more extensive than maybe with the CT shows there's the angiography and then ultimately a post stent placement using the embolic

protection device and overall the trials have shown good good safety met profile overall compared to carotid surgery so it's a minimum minimal exposure not nearly as large the risk of stroke is less because you're not mucking around

up there you're using the best of a low profile system with flow reversal albeit with a mini surgical exposure overall we've actually have an abstract or post trip this year's meeting this is just a snapshot of that you can check it out

this is our one year experience we've had comparable low complication rates overall in our experience so in summary

okay pathophysiology right ventricular the right ventricle is everything when it comes to the pathophysiology of this disease I'm gonna lead you through this because I think it's interesting and important I'm gonna go to this side this

time be fair to both sides of the room so when you have a PE that increases your pulmonary vascular resistance normally the pulmonary vasculature is a very low resistance circuit but when you start putting clots in it it's restive

Gong its its resistance goes up it's kind of analogous to the left an electrical circuit what does that do to the right ventricle well it increases the after load on that right ventricle so what that does is it causes the right

ventricle to blow up like a balloon now by Laplace's law if you take a balloon and you blow it up the intramural pressure is higher in the balloon so if you can imagine that thin walled balloon if you took the pressure at each point

inside of the balloon because it still got a finite thickness the pressure is higher than if it's decompressed now the problem with that is that how does the right ventricle get blood it gets blood from the coronary arteries but if the

pressure inside the ventricle is higher than the pressure differential is less and what what what is Flo rely upon it relies upon a difference in pressure from point A to point B so if that starts to equalize your blood flow to

the right ventricle decreases okay that's why the right ventricle gets ischemic now when the right ventricle becomes ischemic it can't squeeze as hard so it gets hypokinetic when it dilates it also does

not seem to squeeze out as well because the muscle fibers aren't overlapping as well okay so both of those things lead to both so that the right ventricle is now not squeezing is hard and it's not getting blood forward to the left

ventricle so that results in LV preload reduction though LV is not seeing as much blood on top of that when the right ventricle dilates it starts impinging on the left ventricle so now the left ventricular cavity is smaller and it can

accept less blood your output is only as good as your input okay so that's where you start developing systemic hypotension because your left ventricle can't pump out as much blood what happens when your left ventricle can't

pump out as much blood you don't get as much blood into your coronary arteries you don't get as much blood into your coronary arteries you're not getting as much blood into your right ventricle this is the vicious cycle that leads to

right ventricular failure and the progressive death that you see with massive PE now if you were to draw a line like that everything above the line is sub massive PE everything below the line is massive PE okay this is a big

experiment I did we were trying to create sub massive PE we created a massive PE this used to be mostly the L the left-sided chambers and all of a sudden became the right-sided chambers to me this drove home how much the right

side can blow out and dilate that's the only point of this picture I hope I didn't cross you out okay so let's talk

Okay, this is another very delightful category, and I love casing nomenclature. So are these programming letters Greek? It sounds like it. It sounds like a code, VVI, DOO, OVO. But actually, it's a code that's fully understandable.

When I say 32619, you don't even calculate that. You just think, oh, that's today. There's a chart, and you have it in your paperwork. It's the NASPE chart, and this is how programming nomenclature comes about. The first chamber is position I,

and that's the chamber that pace is. So if a patient has several responses, it can pace no chambers, it can pace the A or the atrium, it can pace V or ventricle or it can pace dual, D, which is the atria and ventricle. Position II is the sensing chamber.

And again, it has those same options as a response. Position III, and that's as many as I'm going to go through, is the response to sensing. It has a response to have no response to what is sensed. It has a response to inhabit or to trigger, or it can do D, which is both to inhibit and to trigger.

Now these numbers, letters are used in determining the device programming. There are a few options. One is the option of an inhibitive mode. We don't really use inhibited too much at UVA. However, it's in this consensus statement

so I want to make sure and review it. This is a mode where if native beats occur, the device doesn't pace, it just inhibits. If there is not a native beat sensed, the device will pace and it will pace the appropriate chamber at the rate that its programmed.

The heart rate will be no lower than the set rate. So a patient that is programmed VVI, V is the first position and that's the ventricle. So it tells you that lead is in your ventricle and it would pace the ventricle. The second position is the position that it senses,

which is also the ventricle. Of course it's the lead that, you know, it's in. So it will sense the activity in the ventricle. If it senses that the patient has any of their native beats, it will inhibit or not pace. So that nomenclature is used in general programming,

but these are MRI options as well. Now asynchronous pacing is one that we do use fairly regularly. That patient would be paced at a non-competing rate that's faster than their native rate. So if the patient had a heart rate of 60,

we may or the device nurse would program them to be doing the study at a rate of 80. So the thought is that the patient normally beats at 60 and that's where they've been running, they would override that so to that wouldn't have any need to be paced during that study.

And it paces at this programmed rate. Say they're pacing them at a rate of 80, it will pace regardless of what's happening underneath. It will mostly override it. So probably nothing will happen underneath. But it's going to pace all the time,

and you would anticipate that you would be paced at the programmed rate and now below. Now an example, I'm using the ventricle again. So that second example is VOO. It would pace the ventricle. It would not sense what's happening in the ventricle,

and it would not respond to anything that it of course then sensed. So the other mode is the non pacing mode, and that's a mode for a patient who has a strong underlying rhythm. Maybe they had an ICD implanted

and their ICD was implanted because they had a sudden cardiac death but they have no issues. Or it's just (mumbles) because they're high risk for sudden cardiac death, but no pacing needs. So the pacing indicator or the pacing need is turned off.

So they only have their native rhythm. You would expect that patient to have a variable rate and rhythm because that's what you and I do. All rate response, of course an ICD shocking therapy and tachy therapies are turned off for an MRI, always turned off for an MRI

and I want to mention that again because it's important that we talk over that with the person that's doing the programming prior to their MRI. Now do risks exist for patients that are having an MRI? Yes.

There are concerns, and these concerns are several. One is the device reset with the batteries getting low. So that's why important to make sure that the person has a good battery. Any potential heatings at the lead, at the tissue interface. This is (mumbles) determine to not be

significantly clinically significant. There could be a failure to sense or a failure to pace. Those are some things that we'll talk about. Or inappropriate shocking. Or there is also the option at the device study because of artifacts might increase,

or decrease rather the image quality. Clinical studies however have shown that MRI is safe for both MR conditional and MR nonconditional patients when proper precautions are taken. The risks are rare.

However, with having a well-established monitoring protocol, these risks are minimized, we're prepared for them.

pressure of 60 over 40 minimally responsive I'll give you that

there are probably two right answers if you were going to figure to go by the book on this this PE qualifies as a good I agree with a now what about e somebody pointed this out the other day and I was like oh yeah it's a reasonable point

exactly it has to be greater than 15 minutes so theoretically e is correct as well but that's not what I meant when I put question together all these pitfalls okay

multiple choice question number two seventy year old woman blood pressure of 128 over eighty heart rate of 115 RV strain on echo elevated troponin what type of PE is this I hear a lot of C's that's correct

so let's go through this so yes this person has RV strain on both echo and an elevated troponin so meets that criterion but how do we know the especi is or the passier the especi is positive here the heart rate exactly so the heart

rate on that scale had to be greater than 110 it's 115 so positive especi RV strain and echo elevated troponin high risk intermediate PE 24 year old woman blood pressure of 150 over 80 heart rate of 95 no RV strain large central embolus

what type of PE is this sorry can someone be a little louder dee dee is correct so just the the the thing I was trying to trip you up on is the large central embolus at this point we still do not use where the embolus is as

a criterion for stratification okay now I will say that large central embolus tends to correlate with our V strain so you will see a lot more patients with central embolus have our V dysfunction at the same time and so they'll often

meet the criteria for the sub massive are massive but if you have just a totally normal right ventricle no elevation and the in their troponin and their BNP that is still technically a low risk PE and we'll see this sometimes

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

let me show you a case of massive PE

this launched our pert pert PE response team 30 year-old man transcranial resection of a pituitary tumor post-op seizures intracranial frontal lobe hemorrhage okay so after his brain surgery developed a frontal lobe

hemorrhage and of course few days after that developed hypotension and hypoxia and was found to have a PE and this is what the PE look like so I'll go back to this one that's clot in the IVC right there and

that's clot in the right main pulmonary artery on this side clot in the IVC clot in the right main pulmonary artery systolic blood pressure was around 90 millimeters of mercury for about an hour he was getting more altered tachycardic

he was in the 120s at this point we realized he was not going the right direction for some reason the surgeon didn't want to touch him still to this day not sure why but that was the case he was brought to the ir suite and I had

a great Mickey attending who came with him and decided to start him on pressors and basically treat him like an ICU patient while I was trying to get rid of his thrombus so it came from the neck because I was conscious of this clot in

the IVC and I didn't want to dislodge it as I took my catheters past it and you see the Selective pulmonary and on selective pulmonary angiogram here and there's some profusion to the left lung and basically none to the right lung

take a sheath out to the right side and do an injection that you see all this cast of thrombus you really see no pulmonary perfusion here you can understand why at this point this man is not doing well what I did at this point

was give a little bit of TPA took a pigtail started trying to spin it through aspirated a little bit wasn't getting anywhere he was actually getting worse I was starting to feel very very nervous I had remembered for my AV

fistula work that there was this thing called the cleaner I don't have any stake in the company but I said you know I don't have a lot to lose here and I thought maybe this would be better than me trying to spin a pigtail through

the clock so the important thing about the cleaners it does not go over a wire so you have to take the sheet out then take out the wire then put the cleaner through that sheath and withdraw the sheath

you can't bareback it especially in the pulmonary circulation the case reports are poking through the pulmonary artery and causing massive hemorrhage and the pulmonary artery does not have an adventitia which is the outer layer just

a little bit thinner than your average artery okay so activated it deployed it and you started to get better and this is what it looked like at the end now this bonus question does somebody see anything on this this picture here that

made me very happy on this side this picture here that made me feel like hey we're getting somewhere I'm sorry the aorta the aorta you start to see the aorta exactly and that that was something I was not seen before the

point being that even though this doesn't look that good in terms of your final image the fact that you see filling in the aorta and mine it might have been some of the stuff I had done earlier I can't I can't pinpoint which

of the interventions actually worked but that's what I'm looking for I'm looking for aortic blood flow because now I've got a hole in that in that clot that's getting blood flow to the left ventricle which starts to reverse that RV

dysfunction that we were concerned about make sure I'm okay with time so we'll

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

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 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

other things that we look at tools that we use include the ankle and toe brachial indices those are these at blood pressure comparisons between the

arm and the foot or the toe the great first toe we use segmental pressures your blood pressures and multiple levels down the leg pulse volume recordings which look very similar with cuffs down the leg but they're looking at the size

of the leg per heartbeat PPG's which is basically pulse ox for the four individual toes TCP o2 which is very important and not used enough which is looking at the oxygen tension within the tissue itself and skin perfusion

pressure so ABI as I mentioned as a comparison the arm and the leg pressures and people with CLI often have an ABI less than point for the pressures gonna be less than 50 millimeters in mercury so the ABI may be falsely elevated

people who have chronic kidney disease because the vessels get calcified and they don't compress very well when you blow up the cuff increasing it above 0.45 after if it's been below that is somewhat predictive of wound healing but

not that helpful at the time of an angiogram so as the higher the two pressures is often used to calculate this because you have two pressures and each leg right you have it dorsalis pedis pressure that

you can get and you have posterior tibial so the way that you do in ABI is you look at the higher of the two and compare that to your arm pressure so just remember if your ulcer is being supplied by the vessel that's got the

lower pressure than your ABI is could be normal you could still have CLI so again not always that helpful the toe brachial indices is a it is a little bit more helpful people with diabetes only because the toe arteries tend not to

calcify as quickly in these patients less than 0.75 is considered abnormal and increasing it up into the normal range of course is predictive of fluid wound healing so limitations these only really look at

the macro vascular so that you know the named ves blood vessel patency they don't really tell you what's going on at the level of the capillaries and a recent meta-analysis suggests that neither of them can be consistently

relied upon as okay it came to a normal range we're definitely not gonna get an amputation now so I think I really do have to press both buttons each time so the systolic pressure measurements for segmental pressures you basically look

at the pressures on multiple levels of down the leg a drop of greater than 20 is considered significant and then severity of a number of lesions can't be totally determined from that again this only really tells you what's going on in

the named vessels pulse volume recordings these are cuffs that are looking at the volume of the limb with each pulse it's helpful and patients would they have non compressible vessels because the leg actually has a it's a

microscopic but detectable increase in size with each pulse and so this is better in people who have non compressible vessels and changes in PVR's often will actually precede angiographic findings CTA findings and

recent publication from the s from the society vascular surgery however calls into question their usefulness compared to a bi alone the good pictures are coming soon so this is an example what you may see in

the chart for some of your patients with critical limb ischemia so this is actually segmental pressure and pulse while recording from where I trained in Miami and basically what we're looking at is a combination of things on one of

these sheets so the pressures are listed in the middle but each sheet is going to be different depending on your institution so you're looking for a big drop and pressure from one level to the next so if you look for example in the

middle at the right leg you know there's a 176 in the arm and then there's a 126 in the high thigh normally because of gravity you should have an increase in flow at that level so that's already I have normal on the right side and then

progressing down any grade any drop greater than 20 suggested that something may be abnormal at that level PPG's these are really good for detecting what may be going on at the foot or lower levels so you transmit an infrared

signal through the toe and then try to see how much of that light comes out the other side essentially and so the amount of it it's depending on how much bloods in the digit and the flow the flow of the blood vessels so if you had a

previously flatlined signal then restoring a pulsatile signal is considered a and it you know an approved marker of tissue perfusion so this is essential in patients who have distal ulcers particularly in the level of the

toe because restoring you see you've probably all seen those of you that work in labs that do a lot of peripheral disease seen an angio graphic result where you get flow down to like the mid foot but you see no perfusion down to

the digits and unfortunately that's often not going to be enough to heal a wound so the PPG's are something I try to get in all patients who have tote tote ones so there's an example of a patient who

has flatline and all five digits on the right foot and we recant alized their anterior tibial artery and had flow all the way down there and there was a wound blush in the toe and this is the restore pulsatilla T in all five digits the next

day so at our institution now and also I've modeled after what it was with my training which is the day after the procedure we keep all these patients overnight we get an ABI i segmental pressures and pulsefire

recordings and PPG's and anyone who has flat waveforms in them in their foot level or anybody with a toll sir and if possible we try to get a duplex which you get which I'll go over next it's not always reimbursable at all institutions

if you do them in the same day though so TCP o2 as I mentioned is something that's a little underutilized I think the the task two recommendations that we actually use to stratify the different types of disease and perf arterial

disease suggest that all patients with CLI should have this testing done but it's hard because patients have to not smoke and not drink coffee or tea the morning of the exam and that's hard to get patients to do you have to keep the

room temperature controlled and so it's office availability is limited so an improvement values greater than forty millimeters of mercury in the area surrounding an ulcer suggests that it's going to have successful healing so we

often will do this before we take the patient for an angiogram as a baseline and then bring them back afterwards and if we're if we have a very large increase that you know that's a good sign but of course we're our goal is

usually to be greater than forty and it's one of the few of these tests that's actually useful in patients who don't have Doppler signals so this is a totally not fake wound on this right foot this is example of what it looks

like you basically put multiple probes around the area of the foot and you're testing for the different oxygen tensions skin perfusion pressures is analogous but slightly different basically you're inflating a cop over

different areas of tissue and until the blood flow stops and then slowly deflating it until you can detect light being transmitted through that area again greater than thirty values or predictive of wound healing a lot of

numbers and there will be a test at the end of this so this is a chart kind of showing the ischemic wounds healing likelihood is correlated with an increase in the skin perfusion pressure so if you're less than 30 you're

unlikely to heal if you're greater than 40 it's most likely not an excuse mcquown and you should start looking at other ideologies like venous disease or neuropath neuropathic disease or infection duplex ultrasound is extremely

know we're running a bit short on time so I want to briefly just touch about

some techniques with comb beam CT which are very helpful to us there are a lot of reasons why you should use comb beam CT it gives us the the most extensive anatomic understanding of vascular territories and the implications for

that with oncology are extremely valuable because of things like margin like we discussed here's an example of a patient who had a high AF P and their bloodstream which tells us that they have a cancer in her liver we can't see

it on the CT there but if you do a cone beam CT it stands up quite nicely why because you're giving levels of contrast that if you were to give them through a peripheral IV it would be toxic to the patient but when you're infusing into a

segment the body tolerates at the problem so patient preparation anxa lysis is key you have them exhale above three seconds prior to that there's a lot of change to how we're doing this people who are introducing radial access

power injection anywhere from about 50 to even sometimes thirty to a hundred percent contrast depends on what phase you're imaging we have a Animoto power injector that allows us to slide what contrast concentration we like a lot of

times people just rely on 30% and do their whole the case with that some people do a hundred percent image quality this is what it looks like when someone's breathing this is very difficult to tell if there's complete

lesion enhancement so if you do your comb beam CT know it looks like this this is trying to coach the patient and try to get them to hold still and then this is the patient after coaching which looks like this so you can tell that you

have a missing portion of the lesion and you have to treat into another segment what about when you're doing an angio and you do a cone beam CT NIT looks like this this is what insufficient counts looks like on comb beam so when you see

these sort of Shell station lines that are going all over the screen you have to raise dose usually in larger patients but this is you know you either slow down the acquisition speed of your comb beam or

you raise dose this is what it looks like after we gave it a higher dose protocol it really changes everything those lines are still there but they're much smaller how do you know if you have enhancement or a narrow artifact you can

repeat with non-contrast CT and give the patient glucagon and you can find the small very these small arteries that pick off the left that commonly profuse the stomach the right gastric artery you can use your comb beam CT to find

non-target evaluation even when your angio doesn't suggest it so this is a patient they have recurrent HCC we didn't angio from here those arteries down there where those coils were looked funny even though the patient was

quote-unquote coiled off we did a comb beam CT and that little squiggly C shape structures that duodenum that's contrast going in it this would be probably a lethal event for the patient or certainly would require surgery if you

treated that much with y9t reposition the catheter deeper towards the lesion and you can repeat your comb beam CT and see that you don't have an hands minh sometimes you have these little accessory left gastric artery this is

where we really need your help you know a lot of times everyone's focused and I think the more eyes the better for these kind of things but we're looking for these little tiny vessels that sometimes hop out of the liver and back into the

stomach or up into the esophagus there's a very very small right gastric artery in this picture here this patient post hepatectomy that rides along the inferior surface of the liver it's a little curly cube so and this is a small

esophageal branch so when you do comb beam TT this is what the stomach looks like when it enhances and this is what the esophagus looks like when it enhances you can do non contrast comb beam CTS to confirm ablation so you have

a lesion this is the comb beam CT for enhancement you treat with your embolic and this is a post to determine that you've had completely shin coverage and you can see how that correlates a response so the last thing we're going

thrombectomy is another popular way of treating patients there's a lot of different aspiration catheters the SPX catheter is actually not available currently in the US but what it basically is I can have the rectum a

device that spins in such backlot the Indigo thrombectomy system from penumbra is a yet another device that sucks out clot I think many of us have used that it's kind of like a vacuum cleaner but usually more like a dust

hand vac where it's going to suck up thrombus the angio vac is much more like a Hoover where you're going to use and put a patient on veno-venous bypass that requires a 22 French sheath and a 17 French sheath but that will take out

thrombus I personally prefer using NGO vac in the IVC in big large thrombus for that and not in the pulmonary arteries because it's very inflexible but it's very very useful in a few patient populations in

all of these devices there is no TPA that needs to be given you're just sucking out the clot and you're actually removing it from the patient's body rather than dissolving it and sending it downstream the drawbacks on all of these

devices is their larger access points the SP or X is around six French although that's not that much bigger penumbra device is 8 French and the as we mentioned the angio vac is 22 French

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