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Submassive PE|Peripheral Thrombolysis|66|Female
Submassive PE|Peripheral Thrombolysis|66|Female
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The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
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Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
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Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
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The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
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Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
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Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
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CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
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Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
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Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
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Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
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Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
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Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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Aspiration Thrombectomy | Management of Patients with Acute & Chronic PE
Aspiration Thrombectomy | Management of Patients with Acute & Chronic PE
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The Disease Process | TIPS & DIPS: State of the Art
The Disease Process | TIPS & DIPS: State of the Art
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Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
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CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
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CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
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Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
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Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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Definitions in PE | Pulmonary Emoblism Interactive Lecture
Definitions in PE | Pulmonary Emoblism Interactive Lecture
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Pulmonary Ablation | Interventional Oncology
Pulmonary Ablation | Interventional Oncology
ablationactivitycancercandidatechaptercolorectalcryodiseaselesionslobelungmetastaticnodulepatientpulmonaryrecurrecurredresectionresidualscansurgical
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
anticoagulantanticoagulationcatheterchapterclotcoumadindefensesdirectedheparininpatientintermediatelovenoxNonepatientpatientsplasminogenprocessriskrotationalstreptokinasesystemicsystemicallythrombectomythrombolysisthrombustpa
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
anticoagulationchapterchronicdiseaseDVTdysfunctionechocardiogramembolisminterventionalistsinterventionistsmassivePathophysiologypatientpatientsstatisticsuitesystemicthrombolysisthrombusventricleventricularwilliams
Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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Transcript

of breath at rest. Her symptoms, she quantified as being moderate to severe. She told us she had a little bit of baseline asthma.

This was quite different. She actually had some new right leg swelling, and had been driving from Florida back up to New England. She did have her own history of DVT, but was not on anticoagulants. Other pertinent history, she didn't have any chest pain. She had no fever.

Her past medical history was otherwise positive for hyperlipidemia, and some orthopedic issues primarily. And you can see the rest of the, she was on baby aspirin, that was about it. And then some medications for her orthopedic issues. The timing's important here, so I want you to look at everything.

It's at 7:30 when she was first seen. You can see she's a bit tachycardic. She's 95% on Room Air though. And she's got a good blood pressure. She actually was not in a lot of distress. Her LABS were essentially

negative. But I will point out that, both the troponin and BNP were abnormal in her cardiac profile. She got an EKG perform, and I'd love to give you guys enough time to analyze this, but I'll just cut through the chase quick, and say that, she basically showed some sinus tach. A little bit of right access deviation, and a little bit of ST elevation.

It's a little bit unclear, we did not have an Ovkg. So initially, she was seen by the ER, and the Critical care team. CT of the chest was ordered, of course. She actually had consultation with both VIR and Cardiothoracic surgery, which is sort of our standard protocol.

CT findings, I want everyone to take a look at, pretty clear though if you, I'm gonna come over and try to get this. >> No, it's fine. >> Is it on there? >> Yeah. >> Oh, I'm sorry. So I'll just point out. I think everyone can see the large filling defect.

Here's some axial images that are through the ventricles. Again, I think the findings are pretty clear there. So based upon this clinical scenario, and the imaging findings, which of these is false or incorrect, if you wanna roll

the same question? [BLANK_AUDIO] I'm just gonna read these, they're kinda long. So the patient has clinically significant acute PE, and should be treated with anticoagulation.

Remember which one is false. Patient does not meet the definition of massive PE based on hemodynamic criteria. The patient meets the less common definition of submassive PE, based on obstruction over 75% of the right pulmonary artery.

D, the patient meets the most common definition of submassive PE, based on hemodynamic EKG, lab and CT findings. Or the real tough one, so you gotta think about it, none of these are false. I think we can open the polling. [BLANK_AUDIO]

And I'm gonna do a little bit different, I'm gonna try to go over the answers at the end. But you can show me answer now, it's fine, it's not gotta matter. We're gonna talk about each of these. Each of these is designed to sort of teach a certain point. So the

fact, if we get them wrong, that's good, okay. Looks like most people did pretty well on that. Can you go back to the slides please? So this is real clinical care, and this is what happens with these patients. So over the next five hours, I have the vitals. What I wanna

point out is the difference, that the patient starts out at 7:30 on Room Air. And by the time we're getting toward midnight, we're seeing the patient has progressed to a non-rebreather mask, and then basically on CPAP at the end. So this is happening relatively abruptly. And they have been starting an anticoagulation. Basically,

blood pressure is still maintained. Those are probably the important points there. An echo was obtained. And again, in the interest of time, I'll just show you that the reading was a limited study. But there were suggestions of right ventricular volume overload, and there was actually dilation, and reduced function in the left

ventricle. Those are probably the key findings. Based on the current scenario. Now this one is which one is correct. You can go ahead and show that polling.

>> You got the same question? >> Yeah, I wanna put the next. Yeah, I'll just read this quick. So continued anticoagulation and monitoring is recommended, thrombolysis should never be performed, unless there's hemodynamic compromise. Peripheral thrombolysis

may be performed in such cases. Catheter based thrombolysis, rather than peripheral thrombolysis, should always be performed for this case like this. Or emergent surgical embolectomy, rather than peripheral, or catheter thrombolysis should be performed in cases like this. So let's just roll that poll.

[BLANK_AUDIO] Okay, and we could show the answer. So, sounds like most people are on track there. I'm gonna kinda go through these now, and talk about them a little bit. And the main focus of my talk is gonna be, sort of differentiating massive and submassive PE. These are basically gonna be based on the guide lines. And I

suggest everybody familiarize themselves with these, and they are changing periodically, they're updated every few years. Which one is false. I think people did pretty well here. The one that was false was, this one about the less common definition of submassive PE. Submassive PE is really based on right heart strain, not the

volume of clot seen on PE, although it can be dramatic. And therefore, that was the one that was incorrect. Volume of clot burden has not been predictive of mortality. And that's been shown in a large metanalysis. Just some of the other answers.

Large clot burden, the standard of care is anticoagulation. I don't think anybody would argue with that. Patient with the massive PE criteria, you really need hemodynamic compromise, which our patient did not have at that time. And these are the criteria.

You really have to have a pressure under 90, or sustained blood pressure drop of 40 for 15 minutes, or require basically CPR blood pressure support. Submassive PE is essentially defined, that which produces right heart strain, without producing systemic hemodynamic compromise. That's kind of the key.

And a right heart strain, can be evidenced by many of the findings that we saw, including EKG, echo, CT, or cardiac levels of the blood that we'll talk about. EKG abnormalities, they're talked about a lot, but they're actually fairly non-specific.

And that's one of the problems with them. People talk about the classic pattern which is the S1Q3T3, but it's really seen in less than 20% of cases. In this case, we did have many of the findings, and it was suggestive. But again, EKGs are not specific enough to really

diagnose that. CT really is actually quite good. And again, in this large metanalysis is actually shown to also correlate with mortality, both from PE and all-cause. So CT is very useful. Although again,

the thrombus load is not really predictive of mortality. That's important to keep in mind. But it is associated with adverse clinical outcomes. So you can take that into account, when you're deciding on some of these submassive cases, whether you progress to more aggressive

treatment. Clearly in this case, if we look at the diameters of the right, and left ventricle, and the measurements are there, there was no doubt that this was actually right heart strain. The humoral markers are a little bit like the EKG. And that they're not extremely specific, because as we'll talk about here,

BNP can be elevated, anytime there's any condition stretching the RV. And troponin is really elevated by anything that causes myocardial ischemia. However, in the setting of submassive PE, they are associated with right heart strain,

clinically significant right heart strain. So that's important to keep in mind, they can be useful. Over the next five hours, the patient got more hypoxic, the vital signs got worse. So we have a patient that's declining. The echo, as we talked about, confirmed right heart strain.

This is just to add up something, to orient you a little bit, showing the dilation of the RV, compared to left V. EKG really is the gold standard. Although I have to say, there're some papers on MR now, that are pretty good,

where you actually can get some of these also. The big thing really is diameter, and hypokinesis, or a kinesis actually, which was present in this case. I didn't show you the video to save some time. The next question which again, I think people did pretty well on.

I don't wanna say it's a trick question, but it does make you think, and we'll talk about the answers. The one that was correct is that, peripheral thrombolysis may be performed. It's not mandated, you don't have to do it. And I'm gonna talk about the guidelines, that they're actually very soft on thrombolysis.

So when going through each of these, the patient clearly at this point was still submassive. And the guidelines recommend anticoagulation, not routine thrombolytics, unless you have a protocol. But they are advocated in certain situations. And those certain situations are, that you have a low risk of bleeding, or the initial course or clinical course after anticoagulation, suggests

hypotension or risk of developing it. And it was felt in this case, that this patient was progressing this way. So this is the correct answer for this. Regarding pulmonary artery catheter directed therapy, which is probably what people would rather hear about than this clinical side,

the recommendations are pretty limited if you really read this closely, not because people don't believe in it, because there aren't good randomized-controlled trials to prove it, and they're

very clear about that. Essentially if you're gonna give the lytic, they actually recommend a short two hour infusion, rather than infusing into the main PA. The guidelines recommend, catheter assisted removal for patients with massive PE, and contraindications, failed thrombolysis, or thrombus likely to cause death, all right?.

Now just so we don't all feel bad, surgical embolectomy is in the same boat, because there's not really good randomized trials. And if you look at the recommendations on surgical pulmonary embolectomy, they're actually the same. They recommend contraindications,

failed thrombolysis or thrombus likely to cause death. Now I don't know if you're psychic or how you really know that, cuz if it's that imminent, you're probably in trouble. But that is the guidelines, and that's what you need to be familiar

with. Just a little side on pulmonary embolectomy, we actually have a couple good surgeons. Certain cases are somewhat recommended. So if you have a large right heart burden, that's potentially a case where they do better at, okay.

And the mortality rate has been coming down. So we're fortunate to have a couple of young, impressive surgeons that are available for this. This is just such an example. Just wanted to show you this large burden in the right heart. We decided that we'd send that person to surgery, and they actually

took the smaller stuff out of the left. Just to close it out now, the therapy for the current patient. I just have to show it quick. The patient actually continued to go downhill very rapidly in that last hour.

The TEE confirmed the TTE. She did start to drop her blood pressure. Thus as we talked, she went into the massive category. Basically did the usual. We accessed and went up. In the interest of time, I'll go quickly.

Multimode treatment, we dropped the pressure from about 60, down to about a mean of around 35 or so. We left an infusion catheter in for a few hours. Came back later, her mean pressure was even lower, put a filter in.

She actually got extubated the following day, and believe it or not, went home. So this is to summarize, the guidelines are all evidence based. I suggest everybody really know them, cuz they are right now the key to managing the patients.

I think a pulmonary embolism response team is key, with an algorithm at your institution. I think case by case variation is not good. Your institution needs to manage these, based on the signs that we had. And if you do that, and plan ahead, you will save time, and take good care of patients.

So, I'll leave it at that.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

happy to take any questions or in

ultrasound we don't usually use contrast but one of the procedures were doing for the treatment management of a pulmonary embolism is the ultrasound assisted Rumble Isis do we need contrast so for the thrombolysis is the catheter itself

so you still need to give contrast two to do the procedure but while the catheter is running you don't need to give any contrast four for that is that what you're we don't usually use contrast for ultrasound but

all right when you're treating how will you know that it sliced the clot is less what you frequently do is check the pressures so that catheter allows you to check the pressure and so once you start a patient so you do a pulmonary

angiogram which requires contrast and you put the ultrasound assisted thrombolysis catheter in the eCos catheter then after 24 hours or 12 hours you can measure a pressure directly through that catheter and if the

patient's pressure is reduced you don't have to give them anymore injections yeah and if we are using ultrasound for treatment is it possible to do it for diagnostic purposes No so not for non the prominent artists for

diagnostic imaging unless you're doing an echocardiogram which is technically ultrasound in the heart but for treatment otherwise you need you will need to inject some dye oh thank you

hi I'm Katrina I'm NGH I have one more question okay for your patients with chronic PE do most of them begin with acute PE or if they very separate sort of presentations that's that's a great question so all of them

had acute PE because you can't have chronic without acute but a lot of them are not ever caught so you'll have these patients who had PE that was silent that maybe one day they woke up and had a little bit of chest pain and then it

went away couple days later they thought they had a bronchitis or a cold and then you find out five years later that they had a huge PE that didn't affect them so badly and then they have these chronic findings they usually show up to their

family practice doctor again with hey I just can't walk as far as I can I have a little heaviness they rule them out from a heart attack but it turns out that they have CTF so you you all of them had a Q PE but it takes a lot of time and

effort to find out whether they truly have chronic PE so it's usually in a delayed fashion thank you all right well thank you guys again appreciate it [Applause]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

treatment is the ultrasound assisted catheter director thrombolysis or the echos divisor eCos this technique involves a slow infusion again over 12 to 24 hours

but the catheter has ultrasound built into it and that's thought to help disassociate fibrin strands and to help embed the thrombus bed the TPA into the thrombus I think most people have heard of or seeing eCos in the past

again lower doses much like the catheter directed so it's really the same type of procedure except at the end you're hooking up eCos rather than a uniform Craig Mac there is a lot of differences though in the sort of overall patient

experience because eCos as many of you know requires a lot more devices and for the patient's room so they're gonna have more pumps because it requires more fluid it requires more observation it beeps more frequently overnight but what

I will say is that there are studies that are used that have useful information with eCos and those are actually the main studies that have been done although they're all industry-sponsored but they're very

important studies nonetheless so the only device really that exists for this right now that approved is the eCos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

is my cap nog Rafi reading actually I want to back up a little bit here do I want to back up no I don't I don't want to back up so um let's look at the first

question why is my cap nog Rafi reading abnormal so let's first talk about physiology so a question I get a lot of times is sue the patient comes down for a procedure to the floor I put a sample line set on

them I plug them into the monitor and I'm getting a value of 28 29 30 why are my values abnormal anyone ever see this is anyone still awake okay so there's a few reasons the patients that we are dealing with generally aren't

healthy right I mean sometimes I go to work and I get chest pain I'm like can I just be in an ambulatory gallbladder room today because the patients that are coming from down to IR are sick what their physiology is sick too so we have

Krebs cycle we take oxygen in right it circulates to ourselves it participates in aerobic metabolism we get the byproducts of heat and energy and we get carbon dioxide as a by-product carbon dioxide really diffuse about diffuses

into our blood travels to the lungs and gets exhaled where we measure it so let's talk metabolism really quickly so if someone has a fever if their metabolism is ramped up you think they're gonna be producing more carbon

dioxide yes let's say they're a little hypothermic maybe they're gonna be producing a little bit less you see it for sure in the car patients who are cardiac arrest that are cool to status post cardiac

arrest right those values go way down normal physiology normal physiologic response somebody comes down and they're mildly hypoxic they've got pneumonia or some sort of VQ mismatch and they're hyperventilating to UM debeso

compensate for their hypoxia do you think there's co2 values gonna be a little lower at baseline yeah so these are the patients that you're seeing right so we have reasons that patients could be hyper cap neck like metabolism

right somebody who's in pain someone who's developing a fever early stages of sepsis they may actually have a little bit of a higher value somebody who's sedated or hypoventilating may have a higher value and when we talk about

perfusion is the blood moving round and round is that circulating co2 coming back to the core do we have increased cardiac output with continuous constant ventilation and certainly we can we're gonna look at equipment issues next and

the same goes true more probably in your cases of the hypocapnia patient so someone who is not fully exhaling someone who's in bronchospasm or a COPD or you're not getting that nice square waveform you're only getting some of the

mixed gas ventilation that they're exhaling rights and the conducting airway is mixing with the alveolar gases someone's a little hypothermic someone who's been NPO for 24 hours right it's the opposite of carb-loading right so

you kind of throw them into a little bit of like acidosis you know they're kind of not burning carbs for fuel are they gonna be producing as much carbon dioxide not so much right so when you're coming so when

patients come down to you and you put them on the monitor consider these things so ventilation perfusion gradients so we have what we call our VQ matches and our body is designed beautifully right so when everything is

working great it works great so the way we ventilate all of our lungs owns is very closely matched to the perfusion of all of our lungs ohms so by me standing up here I'd like to think I'm pretty healthy if you did a blood gas and you

put me on one of those filter line sets right now you would hopefully see a gradient that's very small the normal gradient between a PA co2 on a blood gas so the level of carbon dioxide on a blood gas in the arterial blood and what

you see when I fully exhale into the monitor should be between two and five millimeters so these are your patients come down healthy physiology you put them on and you get a value of like 32 then you

could assume that if they were healthy two to five millimeters okay their blood gas would probably like 35 for POC to everyone follow now does any of our patients read the physiology tech books textbooks no they typically don't so

when you have patients come down they may have shunt right so they may have we have our little airway here a and B you're out like picture them as lungs and lung a is blocked so we have no ventilation going to lung a but blood is

still chugging through right so blood is still going through the pulmonary circuit so we're gonna have Patapsco a dia depending on the size of the shunt is this the end of the world are we gonna cancel the case no but just being

aware of the patient's physiology would explain to you why I put this patient on this and I'm getting a value of 30 you follow and it's not the end of the world you document 30 and you monitor for trends as you're going along with your

sedation same thing goes through with dead space dead spaces were ventilating but we have an area of the lung that is not being perfused pulmonary emboli other circulations some medications hypovolemia shocky patients same thing

the VQ mismatch not the end of the world it's part of the patient's physiology maybe part of the reason why they're down there just being aware of these things though so the technology works right our equipment works if just amazed

it's picking up something that we don't connect all the dots on physiologically that sometimes confuses us a little bit so I hope that clears up part of it so when we're monitoring capnography certainly ventilation is what we think

of first and it's important co2 being expired by the lungs that's what we're looking for but if we back up and look at the physiology of carbon dioxide production in the body we are also inferring that

it's being metabolized and being created from Krebs cycle and aerobic metabolism and that we have perfusion occurring okay I'm sure if some of us have seen in our you know nursing careers patients who are kind of peri-arrest and

the capnography kind of drops off it's like a poor man's swan you're watching cardiac output drop in real time because carbon carbon dioxide is not being delivered to the lungs so when we're looking at our patients when

they first come down we first want to establish a baseline value we want to put on a monitor have a patient take some nice deep breaths full ventilations not just one but a few you want to you know have them take a few and look at

their other vital signs their mental baseline status and we're gonna look for trends in their carbon dioxide value so if someone starts off at twenty nine I don't care that they're not 35 to 45 which is textbook normal this person may

not have the stimulus to breathe if I let too much co2 accumulate so we're really looking for the trends okay now somebody will say well how much of you know how much should we look for 10 to 20 percent change from your baseline is

somewhere where you want to start paying attention to what's going on okay maybe like titrating your sedation or just being a little bit more cautious with how much more sedation but again it's more important to look at the trend

value behavior of your carbon dioxide than it is the absolute numbers themselves so first you having a problem let's consider the patient's physiology

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

criteria for CTF means that the patient has a mean pulmonary arterial pressure which we measure intraoperatively exceeding 25 millimeters mercury at rest with the mean pulmonary capillary wedge pressure less than 15 so I'm not a

cardiologist but what that means to me is a mean capillary pulmonary wedge pressure less than 15 means that their left heart is not failing so if you have a capillary wedge pressure higher than 15 that means your left heart is not

working correctly and you can't blame it on the CTF so you can't blame it on the right side if the left side isn't working other things that matter are the abnormal pulmonary vascular resistance and having a systolic pulmonary artery

pressure greater than 40 so what I want to show you and highlight is the law the lost art of pulmonary angiography which i think is now sort of again a lost art some places do a lot of it and some places don't do very much but diagnostic

pulmonary angiography is actually the gold standard in the planning of either surgery or medical management for patients with CTF we do we do these on almost all of our patients with CTF to make that decision with the surgeons and

the cardiologists so the utility is very it's very useful you're able to measure our pressure you're able to decide whether we're the where the thrombus exists in this image here in patients with disease in the

blue and yellow outlined areas those are the patients who can have the operation the operation is curative it's not just medication that you have to take for the rest of your life you can actually remove that chronic clot it's much like

a femoral endarterectomy that are done for patients with peripheral arterial disease although it's a lot more complicated because they have to crack your chest open what's important is getting very very

good high-quality pulmonary angiogram xand so we do we used to do about we do about a hundred of these a year where I trained or actually where I work now and you get very magda up views and you're gonna show all of the vessels and so

these are the views that we use at our institution they happen to be the pipette criteria so it's the same thing you used to do for acute PE you put a flush catheter in the main pulmonary arteries when you're looking at the

upper lobes and when you're looking at the lower lobes you want to push the catheter further into the pulmonary arteries and inject usually what I do is a two to three second injection so that you can stack the images very well and

show all of them in one view this allows your surgeon to make a decision easily as to whether they can operate or they can't operate on this and then I use a higher frame rate usually because these patients are wide awake we when we do

this case we give our patients twenty five mics of fentanyl one time and that's it just to help get the sheath in I usually do this with a seven French sheath and then use a flush cap pulmonary artery catheter many of which

are currently off the market but when we do this we just give them that twenty five Mike's because they have to hold their breath and I usually go up to a high frame rate in the first run and then adjust based off of how well that

patient is holding their breath this really takes a team effort from our nursing technologists and the and the physicians in the room to make sure that this patient does a good job because it's gonna change their management so

there are a lot of different types of angiographic findings on one of these pulmonary angiogram they're really really interesting pulmonary angiogram zin these patients and they're sometimes not at all subtle so you're looking for

a pruning of distal vessels if we start in the top left where you're just not seeing the Brent normal branch pattern you look for stenosis so we're not usually used to looking at stenosis and the pulmonary arteries but this is

actually what you're looking for in CTF you're looking for webs or bands so you'll usually see little areas where you just doesn't look like there's great opacification there's little areas that there's not good at pacification those

are little webs inside the vessel believe it or not looks like a cobweb that grew inside there from that thrombus and then you're looking for areas of complete occlusion that there's just no vessels there those are all

vessels that can be treated in patients with CTF so this is the Jameson classification before we talk about the sort of the interventional management the surgical management is again the curative and dr. Jameson is the head

surgeon at University of California in San Diego which is the largest Palm CTF program in the in the world and he's done I think over 3 500 of these operations I think he's retired at this point but they named the classification

after him and so type 1 is proximal disease so it involves the main pulmonary arteries these are the ideal patients who can get the best benefit from this in their life type 2 is the next best

it's segmental proximal just type 3 is distal segmental and then type 4 is just a mess of sort of all of it but you can't really get a good surgical plane so type 1 and 2 are treated with pulmonary thromboembolism

towards balloon pulmonary angioplasty or BPA and type 4 are generally treated with medication so PT II or pulmonary

strategies so some things that we have

in place right now our peer review Grand Rounds CPOE this is one of my one of my favorite process improvements is is making the right thing the easiest thing and you do that through standardization of processes so that's standard work so

that's your order sets that's the things pop-ups although you don't want to get into pop-up fatigue but pop-ups help our providers for little gentle reminders to guide them to what's right for the patient and to cover everything that we

need we need to cover to ensure the safety of our patient so recently in the fall of last year we had a TPA administration err that occurred it involved a 69 year old patient who two weeks prior had had some stenting in her

right SFA she presented to our clinic when our clinics with some heaviness in her leg and some pain and when she was looked at from an ultrasound standpoint it was determined that her stents were from Bost so she was immediately taken

to the cath lab and it was after angiography did indeed show that there was clot inside these stents they did start catheter directed thrombolysis in the cath lab they also did started concurrent heparin often oftentimes done

with CDT what's usual for our institution is that we have templates that pull in the active problem list for a patient in this case the active problem list or a templated HMP was not used had they

used the template at agent p they would have found that the second active problem on this patients list was a cerebral aneurysm so some physicians will tell you some ir docs will tell you that's an absolute

contra contraindication for TPA however the SI r actually lists it as a relative contraindication so usually we're used to when you when you start a final Isis case you know you're gonna be coming in every 24 hours to check in

that patient in this case we started the the CDT on a Thursday the intent was to bring her back on Monday the heparin many ir nurses will know that we will run it at a low rate usually 500 units an hour and we keep the patient sub-sub

therapeutic on their PTT although current literature will show you that concurrent heparin can also be nurse managed keeping the patient therapeutic in their PTT which is what was done in this case so what ended up the the

course progression of this patient was that so remember we started on Thursday on Saturday she regained her distal pulses in her right leg no imaging Sunday she lost her DP pulse it was thought that it was part of a piece of

that clot that was in the the stent had embolized distally so they made the decision with the performing physicians they consulted him to increase the TPA that was at one milligram an hour to 2 milligrams by Sunday afternoon the

patient had an altered mental status she went to the CT scan which showed a large cerebral hemorrhage they ain't we intubated to protect her airway and by Monday we were compassionately excavating her because

she me became bred brain-dead so in the law there's something that's called the but for argument so the argument can be made that this patient would not have died but for the TPA that we gave her in a condition that she should not have had

TPA for namely that aneurysm so this shows how standard work can be very important in our care of our patients and how standard work drives us down the right way making the easiest thing the safest thing so since that time

we've had a process improvement group that we've established an order set specifically for use and thrombolysis from a peripheral standpoint and then also put together a guideline that was not in place so it's some of that Swiss

cheese that just kind of we didn't have a care set we didn't have a guideline you know we didn't use our template so all those holes lined up and we ended up with a very serious patient safety event so global human air reduction strategies

oops sorry let's go back these are listed in a weaker two stronger and some of what we're using in that case is some checklists so we developed a checklist that needs to be done to cover the

absolute contraindications as well as the relative and it's embedded in the Ulta place order that the physician has to review that checklist for those contraindications and also there to receive a phone call from pharmacy

just to double-check and make sure that they have indeed done that that it's not somebody just checking it off so we have a verbal backup sorry so the just

catheter some other things that we can do is mechanical intervention so if you have a patient usually with massive PE

or the inner or the high-risk B you got to do something to help them out so what we do is put a pigtail catheter and inject a little bit of TPA on the table and then twirl the pigtail or put a wire through the side part of the pigtail and

make it sort of a mechanical fragment fragmentation the problem with that is that fragmented clot goes downstream so when it's in a main pulmonary artery it actually has less surface area than it is when it is in a distal pulmonary

capillary so when you break that clot up you have to be careful because it can actually make the patient worse the benefit there there's no thrombolytic so if we're doing this we we generally are doing it in patients who can't either

receive TPA at all frequently we get patients with who have have had recent spine surgery who get a massive PE had brain surgery get a massive PE and you have to try to treat them without any TPA or even heparin the drawbacks are

that again it increases pulmonary vascular resistance by sending all those little pieces of clot into the small pulmonary arteries and capillaries and it makes it actually much worse in some patients again there's no control trials

and sometimes you need to have a bigger

few different devices and techniques to do this so that everyone sort of again understands what are the different options available to us so you can of course do catheter directed thrombolysis

this can be any of a few different types of catheters so this is an example of a unifier when I talk to the residents and fellows and I just tell them it looks kind of like a garden hose that you poke a bunch of holes in right and you turn

it on and so that's what that looks like you're gonna give delivery of thrombolytic right into the pulmonary arteries ideally you're bathing the pulmonary arteries and you have a catheter on both sides usually on with

two N's one on normal throught normal vessel and the other on the normal vessel in the holes basically embedded in the clot the benefit of this is that you get the drug to the clot very quickly very directly

and you can do it in lower doses than systemic therapy alone the drawbacks are that there are actually no control studies for this there's no randomized control trials that have started everything is a case control series

maybe one institution versus another or within your own institution looking at several things or a registry which I'll show you a few of examples of different types of catheters our unify our Craig McNamara being the two most commonly

used another main mainstay and PE

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

so these are a lot of slides most limited you know I'm talking I'm talking to you guys I'm talking showing you a lot of technical stuff you know and a lot of slides and I'm gonna talk mostly technical of you know how tips and dips are done kind of a step by step so even

the title it's kind of a workshop step by step of how basically you do you do tips and dips and what and and what are they so in general when you have when you have this is basically kind of out flow spleen spleen dumps blood into the

portal vein the mesentery dumps blood into the portal vein portal vein goes into liver liver does its thing and then dumps the blood into the eppadi veins to the right atrium okay for that because the liver is connected with the spleen

and the guts in series unlike any other organ basically the liver has to be a low-resistance organ because the portal circulation is low-pressure look the liver has to be a low-resistance organ with liver disease especially liver

cirrhosis you actually get increased resistance and in the liver with that disease and you get basically a backup of the blood flow in the portal circulation and increases the pressure in the portal circulation that's kind of

the genesis of or the pathogenesis of portal hypertension backing up circulation the spleen and in the guts then you get ascites and hydra thorax that's kind of think of it as weeping of fluid into the pleural space and into

the and into the perineum part of it is oncotic part of is osmotic basically think of it nutritional and pressure driven causes at the same time we all have potential portosystemic connections in other words they're there but they're

not connected or they're not opened up in plumbing they hold them bleed valves or pressure valves when the pressure is high and you know they start weeping or leaking you know in your in your basements we have the same thing

we have so many portosystemic connections there are about 55 named ones there are innumerable ones that are actually that are actually not named the common ones that we know are because of because of bleeding is esophageal

varices that's the connection usually between the left gastric vein and the azekah can be hazardous system you can also get gastric varices and that's usually connecting between a spleen and the left renal vein through a gas renal

shunts you can get also all sorts of connections even down in the internal hemorrhoids we get actually portal hypertension hemorrhoids and bleeding and so many numerous other shunts that we just don't have time to cut to cover

it to cover all these so the general to the general thought of treating all these complications of portal hypertension is to decompress the system to reduce the pressure and that's along the lines of years and decades of

surgery shunts that were placed and now tips ism largely replaced all these surgical shunts with the exception of Vancouver and Tampa okay that they still do some surgical actually a lot of surgical shunts most most other places

in North America converge to a tip to a tip shunt the the advantage of the tips of over surgical shunts is the usual what we hear is minimally invasive it you know it's a quick recovery less morbidity and mortality areason for

white tips has beaten the surgical shunts is the transplant era all these surgical shunts are actually extrahepatic so when you go for a transplants and liver hits the buckets they actually have to go and shut down

these shunts wherever they created them steena renal portal cable in the tips it goes out with a liver in the bucket so there's no complication of transplantation that's the real advantage of tips over surgical shunts

and that's why it's become very very prevalent in in in North America with a transplant error when approaching gastric varices just briefly another way is a BRT Oh which is to go basically into the left renal vein go up the shunt

and specifically screw rows the stomach and that's not the that's not this kind of subject of our of our discussion here I'm gonna talk to you

to talk about is indirect angiography this is kind of a neat trick to suggest to your intervention list as a problem solver we were asked to ablate this lesion and it looked kind of funny this patient had a resection for HCC they

thought this was a recurrence so we bring the comb beam CT and we do an angio and it doesn't enhance so this is an image here of indirect port ography so what you can do is an SMA run and see at which point along the

run do you pacify the portal vein and you just set up your cone beam CT for that time so you just repeat your injection and now your pacifying the entire portal vein even though you haven't selected it and what to show

well this was a portal aneurysm after resection with a little bit of clot in it the patient went on some aspirin and it resolved in three months so back to our first patient what do you do for someone who has HCC that's invading the

heart this patient underwent 2y 90s bland embolization microwave ablation chemotherapy and SBRT and he's an eight-year survivor so it's one of those things where certainly with the correct patient selection you can find the right

things to do for someone I think that usually our best results come from our interdisciplinary consensus in terms of trying to use the unique advantages that individual therapies have and IO is just one of those but this is an important

lesson to our whole group that you know a lot of times you get your best results when you use things like a team approach so in summary there are applications to IO prior to surgery to make people surgical candidates there are definitive

treatments ie your cancer will be treated definitively with curative intent a lot of times we can save when people have tried cure intent and weren't able to and obviously to palliate folks to try to buy them time

and quality of life thermal ablation is safe and effective for small lesions but it's limited by the adjacent anatomy y9t is not an ischemic therapy it's an ablative therapy you're putting small ablative radioactive particles within

the lesion and just using the blood supply as a conduit for your brachytherapy and you can use this as a new admin application to make people safer surgical candidates when you apply to the entire ride a panic globe

thanks everyone appreciate it [Applause] [Music]

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

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

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

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

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

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

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

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

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

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

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

of these issues filters are generally still use or were used up until a few years ago or five years ago almost exclusively and then between five years and a decade ago there was this new concept of proximal protection or flow

reversal that came about and so this is the scenario where you don't actually cross the lesion but you place a couple balloons one in the external carotid artery one in the common carotid artery and you stop any blood flow that's going

through the internal carotid artery overall so if there's no blood flowing up there then when you cross the lesion without any blood flow there's nothing nowhere for it to go the debris that that is and then you can angioplasty and

or stent and then ultimately place your stent and then get out and then aspirate all of that column of stagnant blood before you deflate the balloons and take your device out so step-by-step I'll walk through this a couple times because

it's a little confusing at least it was for me the first time I was doing this but common carotid artery clamping just like they do in surgery right I showed you the pictures of the surgical into our directa me they do the vessel loops

around the common carotid approximately the eca and the ICA and then actually of clamping each of those sites before they open up the vessel and then they in a sequential organized reproducible manner uncle Dee clamp or unclamp each of those

sites in the reverse order similar to this balloon this is an endovascular clamping if you will so you place this common carotid balloon that's that bottom circle there you inflate you you have that clamping that occurs right

so what happens then is that you've taken off the antegrade blood flow in that common carotid artery on that side you have retrograde blood flow that's coming through from the controller circulation and you have reverse blood

flow from the ECA the external carotid artery from the contralateral side that can retrograde fill the distal common carotid stump and go up the ica ultimately then you can suspend the antegrade blood flow up the common

carotid artery as I said and then you clamp or balloon occlude the external carotid artery so now if you include the external carotid artery that second circle now you have this dark red column of blood up the distal common carotid

artery all the way up the internal carotid artery up until you get the Circle of Willis Circle of Willis allows cross filling a blood on the contralateral side so the patient doesn't undergo stroke because they've

got an intact circulation and they're able to tolerate this for a period of time now you can generally do these with patients awake and assess their ability to tolerate this if they don't tolerate this because of incomplete circle or

incomplete circulation intracranial injury really well then you can you can actually condition the patient to tolerate this or do this fairly quickly because once the balloons are inflated you can move fairly quickly and be done

or do this in stepwise fashion if you do this in combination with two balloons up you have this cessation of blood flow in in the internal carotid artery you do your angioplasty or stenting and post angioplasty if need be and then you

aspirate your your sheath that whole stagnant column of blood you aspirate that with 320 CC syringes so all that blood that's in there and you can check out what you see in the filter but after that point you've taken all that blood

that was sitting there stagnant and then you deflate the balloons you deflate them in stepwise order so this is what happens you get your o 35 stiff wire up into the external carotid artery once it's in the external cart or you do not

want to engage with the lesion itself you take your diagnostic catheter up into the external carotid artery once you're up there you take your stiff wire right so an amp lats wire placed somewhere in the distal external carotid

artery once that's in there you get your sheath in place and then you get your moment devices a nine French device overall and it has to come up and place this with two markers the proximal or sorry that distal markers in the

proximal external carotid artery that's what this picture shows here the proximal markers in the common carotid artery so there's nothing that's touched that lesion so far in any of the images that I've shown and then that's the moma

device that's one of these particular devices that does proximal protection and and from there you inflate the balloon in the external carotid artery you do a little angiographic test to make sure that there's no branch

proximal branch vessels of the external carotid artery that are filling that balloon is inflated now in this picture once you've done that you can inflate the common carotid artery once you've done that now you can take an O on four

wire of your choice cross the lesion because there's no blood flow going so even if you liberated plaque or debris it's not going to go anywhere it's just gonna sit there stagnant and then with that cross do angioplasty this is what

it looks like in real life you have a balloon approximately you have a balloon distally contrast has been injected it's just sitting there stagnant because there's nowhere for it to go okay once the balloons are inflated you've

temporarily suspends this suspended any blood flow within this vasculature and then as long as you confirm that there's no blood flow then you go ahead and proceed with the intervention you can actually check pressures we do a lot of

pressure side sheath pressure measurements the first part of this is what the aortic pressure and common carotid artery pressures are from our sheath then we've inflated our balloons and the fact that there's even any

waveform is actually representative of the back pressure we're getting and there's actually no more antegrade flow in the common carotid artery once you've put this in position then you can stent this once the stent is in place and you

think you like everything you can post dilated and then once you've post dilated then you deflate your balloon right so you deflate your all this debris that's shown in this third picture is sitting there stagnant

you deflate the external carotid artery balloon first and then your common carotid artery and prior to deflating either the balloons you've aspirated the blood flow 320 CC syringes as I said we filter the contents of the third syringe

to see if there's any debris if there's debris and that third filter and that third syringe that we actually continue to ask for eight more until we have a clean syringe but there's no filter debris out because

that might tell us that there's a lot of debris in this particular column of blood because we don't want to liberate any of that so when do you not want to use this well what if the disease that you're dealing with extends past the

common carotid past the internal carotid into the common carotid this device has to pass through that lesion before it gets into the external carotid artery so this isn't a good device for that or if that eca is occluded so you can't park

that kampf balloon that distal balloon to balloon sheath distally into the external carotid artery so that might not be good either if the patient can't tolerate it as I mentioned that's something that we assess for and you

want to have someone who's got some experience with this is a case that it takes a quite a bit of kind of movement and coordination with with the physician technologists or and co-operators that

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

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

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

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

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

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

systemic TPA so I wanted to go through a

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

blasian it's well tolerated and folks with advanced pulmonary disease there's a prospective trial that showed that

there are pulmonary function does not really change after an ablation but the important part here is a lot of these folks who are not candidates for surgical resection have bad hearts a bad coronary disease and bad lungs to where

a lot of times that's actually their biggest risk not their small little lung cancer and you can see these two lines here the this is someone who dr. du Puy studied ablation and what happens if you recur and how your survival matches that

and turns out that if you recur and in if you don't actually a lot of times this file is very similar because these folks are such high risk for mortality outside or even their cancer so patient selection is really important for this

where do we use it primary metastatic lesions essentially once we feel that someone is not a good surgical candidate and they have maintained pulmonary function they have a reasonable chance for surviving a long

time we'll convert them to being an ablation candidate here's an example of a young woman who had a metastatic colorectal met that was treated with SPRT and it continued to grow and was avid so you can see the little nodule

and then the lower lobe and we paste the placement prone and we'd Vance a cryo plugs in this case of microwave probe into it and you turn off about three to five minutes and it's usually sufficient to burn it it cavitate s-- afterwards

which is expected but if you follow it over time the lesion looks like this and you say okay fine did it even work but if you do a PET scan you'll see that there's no actually activity in there and that's usually pretty definitive for

those small lesions like that about three centimeters is the most that will treat in a lot of the most attic patients but you can certainly go a little bit larger here's her follow-up actually two years

that had no recurrence so what do you do when you have something like this so this is encasing the entire left upper lobe this patient underwent radiation therapy had a low area of residual activity we followed it and it turns out

that ended up being positive on a biopsy for additional cancer so now we're playing cleanup which is that Salvage I mentioned earlier we actually fuse the PET scan with the on table procedural CT so we know which part of all that

consolidated lung to target we place our probes and this is what looks like afterwards it's a big hole this is what happens when you microwave a blade previously radiated tissue having said that this

was a young patient who had no other options and this is the only side of disease this is probably an okay complication for that patient to undergo so if you follow up with a PET scan three months later there's no residual

activity and that patient actually never recurred at that site so what about

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

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

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

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