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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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What's Next | AVIR CLI Panel
What's Next | AVIR CLI Panel
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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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Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
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The Expanded Role for Radiology Nursing | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
The Expanded Role for Radiology Nursing | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
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General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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Combining Guidelines with What You Know | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Combining Guidelines with What You Know | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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What type of PE is this? | Pulmonary Emoblism Interactive Lecture
What type of PE is this? | 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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Programming for MRI  | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
Programming for MRI | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
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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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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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Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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CRT Therapy or Bi-Ventricular Devices | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
CRT Therapy or Bi-Ventricular Devices | Demystifying (Cardiac) Device Monitoring for MRI Studies: The Expanded Role of Radiology Nursing
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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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 Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
Q&A Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
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The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
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Where We Are Now | Pulmonary Emoblism Interactive Lecture
Where We Are Now | Pulmonary Emoblism Interactive Lecture
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Normal Bleeding | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Normal Bleeding | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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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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Non-Invasive Ventilation | Respiratory Compromise: Use of Capnography During Procedural Sedation
Non-Invasive Ventilation | Respiratory Compromise: Use of Capnography During Procedural Sedation
accurateairwaychaptercircuitcolorconsistentcpapdatadevicesdistaldistallyleaklevelliterlitersmaskmonitoringnasalNoneoraloxygenationpatientpatientsportprettysamplingstentsupplementalvaluesventilationventilator
Outcome data | Uterine Artery Embolization The Good, The Bad, The Ugly
Outcome data | Uterine Artery Embolization The Good, The Bad, The Ugly
arterybleedcentimeterchapterdatadysfunctionalembolizationfertilityfibroidfibroidsMRImyomectomyNonepatientsretainsurgeryuterineuterus
Treatment Options- CAS- Embolic Protection Device (EPD)- Distal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Distal Protection | Carotid Interventions: CAE, CAS, & TCAR
arteriesarteryaspirateballoonbasketbloodbraincapturecarotidcarotid arterycerebralchapterclinicaldebrisdevicedistaldistallyembolicfilterfiltersflowincompleteinternalinternal carotidlesionlesionsoversizeparticlespatientperfectphenomenonplaqueprotectedprotectionproximalsheathstenosisstentstentingstrokestrokesthrombustinyultimatelyvesselwire
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
angiographyangioplastyarterybleedbloodcalcifiedcarotidchapterclaviclecommondebrisdevicedistalembolicembolizationexposurefemoralflowimageincisioninstitutionlabeledpatientprocedureprofileproximalreversalreversesheathstenosisstentstentingstepwisesurgicalsuturedsystemultimatelyveinvenousvessel
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
angioplastyantegradearteryaspirateballoonballoonsbloodcarotidcarotid arterychaptercirclecirculationclampclampingcolumncommoncontralateralcrossdebrisdeflatedevicedevicesdilateddistaldistallyexternalexternal carotidfilterflowincompleteinflateinflatedinternalinternal carotidlesionmarkerspatientpressureproximalretrogradesheathstentstepwisesyringesyringestoleratevesselwilliswire
The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
aspiratecathetercatheterizedchapterdatadeviceembolismenrollmentinflectionmassiveoptimizedpatientspulmonaryrandomizedsystemicthrombolysisthrombolyticsthrombustrialtrials
Transcript

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

So the full title of this statement

that changes everything is the 2018 HRS, that's the Heart Rhythm Society, Expert Consensus Statement on MRI Imaging and Radiation Exposure in Patients with CIEDs. Those are cardiovascular implantable electronic devices. And this guideline is intended to provide

useful and practical recommendations for patients so that they can safely undergo imaging and treatment. It's not intended to dictate management of details that they state are best left to the individual institutions to develop.

The Heart Rhythm Society and 11 other national and international colleges collaborated to write this statement. They included experts from the American College of Cardiology, the American College of Radiology,

the American Heart Association, people from Europe and Peru. And these were experts that were saying, "Okay, we've got these patients that need MRIs. "What are we going to do about it?" And one of their statements,

and the one that actually changed everything for us, was, "It is recommended that personnel "with the skill to perform advanced cardiac life support, "including the expertise in arrhythmia recognition, "defibrillation and transcutaneous pacing "accompany that patient."

So this means that qualified radiology nurses can monitor device patients. So what's the big deal? Radiology nurses have extensive training in the care and safety of patients in radiology and in MRI.

However, understanding of pacemakers and defibrillators and the potential issues that can occur are not necessarily a part of the radiology nurse background. In caring for these patients that are having their MRI device studies,

nurses need to be prepared. Radiology nurses need to be prepared.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

and I'm gonna let Carrie go over a case study with you all we printed and gave you one of those and this is just gonna

kind of really show you the importance of yes let's have established guidelines to help guide nursing practice but then let's also take into consideration what we know so I'll just give you all a minute to look over the the patient I'm

not going to read this all to you what's the journal was 28 to the right is right here June 2018 volume 37 number 237 number 2 June 2018 and it's bolded in our reference side - so here's the time for audience feedback if you are a

nurse and you saw this patient what are some things that might concern you about them heading into a procedure there's microphone if anybody wants it or you can just call out liver dysfunction when we were looking

at this patient and this is you know an actual patient that I saw doing a workup and said hmm this is a really complex patient what are we going to do with this person they are having a lowest procedure as Nicky points out so that is

good to note in this patient was actually admitted following a stroke while anticoagulation was being held for another low-risk procedure so that's definitely something that caught our attention and we looked at our lab

values again the INR pretty normal they were taking lovenox at home but they're currently in the hospital they're on IV heparin and a lot of our procedures come up at the last minute so this is it's not uncommon

for us to show up in the morning have half of our day filled and have cases added as the day goes on and I would imagine that's pretty much the standard for most of you so and they wanted this today this was more of a therapeutic

procedure but they really did want it for the patient so we got out our nursing guideline we looked at what medications are they on what's their history what does our guideline tell us and I've included the low-risk procedure

and it tells us IV heparin hold for four hours so normally the nurse would call the floor and say can you have a discussion with your service would you know can they hold the heparin per our procedural guidelines in this case we

didn't feel like it was a good idea to have that nurse to nurse conversation this is a case where we went directly to the radiologist and said here's the patient here's what our guidelines tell us could you please call the service and

have a conversation with them and they did they talked about the risks and benefits you know in our practice we do occasionally do procedures with IV heparin running it's been known to happen it's definitely not preferred but

again it's that risk benefit decision in this case the service felt it would be okay to hold the heparin for four hours the radiologist agreed that they would be okay with and so the heparin was turned off the

flora nurse called us when they turned it off we verified it in the medical record transport order was put in the patient was brought down at exactly four hours and the procedure was performed successfully the patient was returned

directly to the floor and the heparin restarted but we just picked this one as just an interesting patient to look at because it does show we have these guidelines they encourage nurses to look at these things while we're screening

patients but we also need to think critically and say you know does this warrant a little bit of extra consideration should the radiologist and the service have this conversation or is the service managing the patient going

to do what our recommendations say so we do run into this kind of thing quite often and they did say at the session this morning nurses want a guideline but there's no cookbook for these patients and I think that emphasizes that we can

make all the screening guidelines in the world they're very helpful for streamlining triaging patients getting patients in but ultimately we're going to have a lot of these multidisciplinary conversations where radiologists are

talking to the service that's managing the patient and flora nurses radiology nurses everybody is getting involved in the conversation so it's really kind of a collaborative approach even though we do have these guidelines they don't

apply for every situation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

it's obviously either done with general

anesthesia or perhaps a regional block at our institution is generally done with general anesthesia we have a really combined vascular well developed combined vascular practice we work closely with our surgeons as well as

you know those who are involved in the vascular interventional space as far as the ir docs and and in this setting they would do generally general anesthetic and a longitudinal neck incision so you've got that and the need for that to

heal ultimately dissect out the internal carotid the external carotid common carotid and get vessel loops and good control over each of those and then once you have all of that you hyper NIH's the patient systemically not unlike what we

do in the angio suite and then they make a nice longer-term longitudinal incision on the carotid you spot scissors to cut those up and they actually find that plaque you can see that plaque that's shown there it's you know actually

pretty impressive if you've seen it and let's want to show an illustrative picture there ultimately that's open that's removed you don't get the entirety of the plaque inside the vessel but they get as much as they can and

then they kind of pull and yank and that's one of the pitfalls of this procedure I think ultimately is you don't get all of it you get a lot more than you realize is they're on on angiography but you don't get all of it

and whatever is left sometimes can be sometimes worse off and then ultimately you close the wound reverse the heparin and closed closed it overall and hope that they don't have an issue with wound healing don't have an issue with a

general anesthetic and don't have a stroke in the interim while they've clamped and controlled the vessel above and below so here's a case example from our institution in the past year this is a critical asymptomatic left internal

carotid artery stenosis pretty stenotic it almost looks like it's vocally occluded you can see that doesn't look very long it's in the proximal internal carotid artery you can see actually the proximal external carotid artery which

is that kind of fat vessel anteriorly also looks stenotic and so it's going to be addressed as well and this is how they treated it this is the exposure in this particular patient big incision extractors place and you can see vessel

loops up along the internal and external carotid arteries distally along some early branches of the external carotid artery off to the side and then down below in the common core artery and ultimately you get good vessel control

you clamp before you make the incision ultimately take out a plaque that looks like this look how extensive that plaque is compared to what you saw in the CT scan so it's not it's generally much more

impressive what's inside the vessel than what you appreciate on imaging but it's the focal stenosis that's the issue so ultimately if yet if the patient was a candidate stenting then you just place a stent

across that and he stabilized this plaque that's been removed and essentially plasti to that within the stent so it doesn't allow any thrombus to break off of this plaque and embolize up to the brain that's the issue of raw

it's the flow through there becomes much more turbulent as the narrowing occurs with this blockage and it's that turbulent flow that causes clot or even a small amount of clot to lodge up distally within the intrical in

terrestrial vasculature so that's the issue here at all if you don't take all that plaque out that's fine as long as you can improve the turbulent blood flow with this stent but this is not without risk so you take that plaque out which

looks pretty bad but there are some complications right so major minor stroke in death an asset which is a trial that's frequently quoted this is really this trial that was looking at medical therapy versus carotid surgery

five point eight percent of patients had some type of stroke major minor so that's not insignificant you get all that plaque out but if you know one in twenty you get a significant stroke then that's not so bad I'm not so good right

so but even if they don't get a stroke they might get a nerve palsy they might get a hematoma they may get a wound infection or even a cardiovascular event so nothing happens in the carotid but the heart has an issue because the

blockages that we have in the carotid are happening in the legs are happening in the coronary so those patients go through a stress event the general anesthetic the surgery incision whatever and then recovery from that I actually

put some stress on the whole body overall and they may get an mi so that's always an issue as well so can we do something less invasive this is actually a listing of the trials the talk is going to be available to you guys so I'm

not going to go through each of this but this is comparing medical therapy which I started with and surgery and comparing the two options per treatment and showing that in certain symptomatic patients if they have significant

stenosis which is deemed greater than 70% you may be better off treating them with surgery or stenting than with best medical therapy and as we've gotten better and better with being more aggressive with best medical therapy

this is moving a little bit but here's the criteria for treatment and so you have that available to you but really is

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

Now a special category of device monitoring is patients who have cardiac resynchronization therapy or CRT, or it's a biventricular device. A lead goes into both the right and left ventricle. And I'll just tell you about this so that you,

it doesn't change our device monitoring really. However, it's something that you'll hear about. And a person with a low ejection fraction is a candidate for this. They have a wide QRS complex. It means as that muscle is big,

like cardiomyopathy or someone who has a large heart muscle, the conduction from south to south to south takes longer and so they have a wide QRS complex. A third lead is implanted so that it paces the right ventricle synchronized with the left ventricle.

And the goal is to have the left ventricle contract more efficiently and uniformly. By beating symmetrically, it helps to improve the ejection fraction. The heart pumping action is improved. And it mimics, resynchronization mimics

healthy heart contractions. Okay, now don't be afraid (chuckles) but it's quiz time. If a patient had complete heart block, just think, what kind of device would they have? They just have complete heart block. Ideas? Think about it.

They would have a pacemaker. If someone has tachy brady syndrome, sometimes fast, sometimes slow but their ejection fraction is norm, it's normal, it's 50%? Maybe a little on the low side, but what type of device would they have?

(indistinct chattering) Excellent. A patient who has survived sudden cardiac death, what type of (mumbles)? (indistinct chattering) ICD. Now if a patient has congestive heart failure and an ejection fraction that's low, it's 15%,

what type of device would they qualify for? (indistinct chattering) They would have an ICD. They would have an ICD, and they may need pacing indications. Right now we don't know that by just their diagnosis.

However, this patient has congestive heart failure and they have a sick sinus syndrome so they have maybe a low heart rate that they're not tolerating very well and their ejection fraction is above 35%, it's 40%. What would they have?

(indistinct chattering) You guys are good. I must be saying it right. If they have only need for pacing, they'll have a pacemaker. If they have a need for pacing and they have a risk for sudden cardiac death or they've had a prior event of sudden cardiac death,

they would have a defibrillator placed. And that patient, if they had the pacing indication, would utilize those pacing functions of their ICD. So remember, all ICDs can do everything a pacemaker can do. ICDs can pace, but pacemakers cannot shock. Sometimes a patient, and this is why I'm sort of saying this

because there is a little misunderstanding, they come in in there insistent they have a pacemaker and an ICD. Well, no. They don't, they actually have an ICD that's doing both functions.

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

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

questions comments and accusations please hello this topic is very personal to me I've had it actually had a UFE so this is like one of my big things I work in the outpatient center as well as a

hospital where we perform you Effy's and frequently the radiologist will have me go in and talk to the patient it's from a personal perspective one of the issues which it may just have been from my situation was pain control post UFE

whether you normally tell your patients about pain control after the UFE someone say we are all struggling with this yeah oh it's not what's your question is going to be okay good I'm gonna get doctor Dora to answer Shawn the question

is what do you what do we do with this pain issue you know what are you doing for the home there at Emory there you know and a lot of practices we we don't rely on one magic bullet for pain control recently we've been doing

alternate procedures for two adjunctive procedures to help with pain control for example there are nerve blocks that you can do like a superior hypogastric nerve block there's there's Tylenol that can be given intravenously which is seems to

be a little more effective than by mouth there's there's a you know it and a lot of times it's it's a delicate balance right between pain post procedural pain because you can often get the pain well controlled with with narcotics opioid

with a pain pump but the problem is 12 hours later the patients is extremely nauseous and that's what keeps her in the hospital so it's a it's a balance between pain control and nausea you can you can hit the nausea

beforehand using a pain and scopolamine patch that that'll get built up in the system during the procedure and that kind of obviates the nausea issues like I said that the the nerve blocks the the tile and also there are some other

medicines that can can be used adjunctive leaf or for pain control in addition to to the to the opioids so the answer the question is there are multiple there multiple answers to the question there's not one magic bullet so

that helped it did one of the things that I tell the patients is that you know everyone is different and yet some people I've seen patients come out and they have no pain they're like perfect and then some come out and they are

writhing in the bed and they're hurting and they're rolling all around what and I always ask the acid docs are you telling them they could possibly have you know pain after the procedure because some have the expectation that

I'm going to be pain-free and that's not always the case so they have an unrealistic expectation that I'm gonna have the UFE but not have pain what I also tell them is that the pain it's kind of like an investment right and

this is easy for a guy to say that right but but it's it's an investment the worst part the worst pain you should be feeling is the first 12 12 hours or so every day I tell my patient you're gonna be getting better and better and better

with far as the pain as long as you is you follow our little cookbook of medicines that we give you on the way home and I want you to make sure that you fill these prescriptions on the way home or you have someone fill those

prescriptions for you before he or she picked you up in the hospital and lately we have been and I see that you're there as well lots of other little tricks that are out there right and again there are all

little tricks so ensure arterial lidocaine doctor there is near alluded to and if you're on si R Connect you may it may spill over on some of your chat rooms here people have been using like muscle relaxant like flexural or

robertson with some success but just know that we don't have any studies that tell us how that's supposed to do so when i have someone that is like writhing in pain i just use everything so i do it superior hypogastric nerve

vlog and i actually will do some intra-arterial lidocaine although not so much lately i have been using the muscle relaxant but i will warn you that i've had two patients with extreme anticholinergic effects where they are

now not able to pee from that so you know where we're doing that balance act I see that you're there can I take that question here first just so we're we're doing the same thing we're using the multimodal just throwing all these

things at people and we're trying the superior hypogastric blocks but we're collaborating with anesthesia to do that right now do you all do your own blocks or do you collaborate with anesthesia we do our own blocks okay it isn't it is

not that difficult I would tell you that but again it's kind of like you know you got to do if you start feeling better and then you're like we don't really need them we'll just do it on our own okay thank you again yes what's the

acceptable interval between UFE and for IBF oh that's a your question what is the interval between UFE and IVF so if you wanted to get pregnant yeah and can you have a you Fe and then have an IVF like how long would you have to wait

wait and tell you before you can have that the IBF it I guess it really depends on the age of the patient because we know that that the threshold for which patient tend to have that inability to conceive

is around 45 years old so you know it did below the you know below the age of 45 the risk of causing ovarian failure or or the inability to conceive is significantly less it's zero zero to three percent so I would say that you

know you probably want the effects of the fibroid embolization to two to take effect it takes around 12 months for these fibroids to shrink down to their most weight that they're gonna they're going to shrink down the most I wouldn't

say you need to wait 12 months to put our nine vitro fertilization there's no good there's no good literature out there I don't believe that's your next and so I would say just remember that if you came to my practice and you said you

wanted to get pregnant I will be sending you to talk to fertility specialists beforehand we do not perform embolization procedures as a way to become pregnant there's no data to support that but if you saw your

gynecologist and they said let's do this then I'm sure they'll be doing lots of adjunct things to figure out what would be an ideal time then to for you to have IVF and if I dove not having any data to inform me I would ask you to wait a year

and what will be the effect of those hormones that they gave you if for example a patient has existing fibroids what would be the effect of those hormones that IVF doctors prescribed their patients yeah so fibroids actually

can grow during pregnancy so I would say that most of those hormones are pro fertility hormones so I would expect that maybe you can see some of that effect as well yeah alright if you have any other questions you can grab me oh

you're I'm sorry go with it okay yes we we have time I don't want to keep anybody here for that so I have a two-fold question the first one is post-procedure can you use a diclofenac patch or a 12-hour pain

patch that is a an NSAID have you have any experience with that and your next question my second part of the question is there a patient profile or a psychological profile that tips you that the patient is not going to be able to

candidate because of their issues around pain so they're two separate but we have in success sending people home that first day so I'm looking to just make it better I haven't had experience with the Clos

phonetic patch it's in theory it seems ok you know these are all the these are they're all these are non-steroidal anti-inflammatory drugs so there are different potency levels for all of them they you know they range from very low

with with naproxen to to a little bit higher with toradol like that clover neck I think is somewhere in between so we found that at least I found that that q6 our our tour at all it tends to help a lot so with that said I I don't have

much experience with it with the patch in answer to your second question the only thing I can say is there there is a strong correlation between size of fibroids and the the amount of a post procedural pain and post embolization

syndrome so there really you know we often say we don't really care too much about the number of fibroids but the size of the fibroid is is is should be you know you should you should look at that on pre procedural imaging because

if it gets too big it may not be worth it for the patient because they may be in severe pain the more embolic you put into the blood supply's applying the the fibroid the the greater the pain post procedural pain

are there multiple other factors that would contribute to pain but that's that's one aspect you can you can look at post procedurally on imaging okay thank you very much yes ma'am hi what what kind of catheter do you use

to catheterize the fibroid artery when you pass by radio access yeah so over the last three years the companies have been really very good about that so there are a few things that I without endorsing one company or the other that

you need to make sure that the sheath that you're using is one of those radial sheets a company that makes a radio sheath you should not use a femoral sheath for radial access so no cheating where that's concern you may get away

with it once or twice but it will catch up to you and you need a catheter that is long enough to go from the radio to the to the groin so I'm looking for like a 120 or 125 centimeter kind of angled catheter whether it's hydrophilic the

whole way or just a hydrophilic tip or not at all you can you can choose which one in our practice most of us still tend to use a micro catheter through that catheter although if I'm using a for French and good glide calf and it

just flips into like a nice big juicy uterine artery then I may just go ahead and take that and do the embolization if the fellow is not scrubbed in as well so thanks a lot but they make they make many different kinds like that and more

of those are to come all right I'm you can please please please send us any other questions that you have thanks for your time and attention and enjoy the rest of the living

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

so where we are now these are my concluding slides massive PE is lethal systemic lysis should be used surgery should be discussed immediately in the ECMO which I didn't really get a chance

to talk about it's probably a game-changer because it's almost like a temporizing measure for any of these therapies patient comes in you immediately put them on cardiopulmonary bypass support and then you can decide

what to do should this patient get an embolectomy should this patient get a free directive therapy should we just wait and let the patient write it out and that is a right answer actually just keep them an anticoagulation so this

will be a game-changer for massive PE sub massive PE is dangerous to some of the patients risk benefit of systemic thrombosis is not favorable for most but for some it might be and CDT appears to be promising but we have a lot of work

to do so where we need to go from here is that I think for mass pe we need a prospective registry and we really need a randomized control trial for CDT for sub massive PE thank you very much guys thanks for your attention

Kerry go into kind of a refresher from

this morning for you all this is a video from a liver biopsy and let's just start that no we actually don't know how to play this from the clicker okay

so this is just a short clip to show normal bleeding everybody bleeds and all the procedures that we do involve placing needle in the patient so we are going to have some amount of bleeding and it can range from seconds to minutes

and hopefully it's a fairly minimal amount of blood loss typically what happens is the needle is inserted into the patient the body detects the injury clotting mechanisms are activated hemostasis is restored which sounds

pretty simple but as you may remember from this morning there are a lot of different mechanisms involved that make that happen and we wanted to just provide a brief overview for those of us that have been out of nursing school for

a little while so we thought it would be helpful to start with just a brief generalized overview the first step obviously is the endothelial injury platelet plug forms the coagulation cascade starts we get a clot and then we

have the Ambo thrombotic control mechanisms and the fibrinolysis in our practice we're really just concerned with the first two we really just want to make sure that the patient has the ability to clot so here's a fairly

simplified version of the coagulation cascade the factors are the Roman numerals and to keep it simple we've just included a few of them so we have a wound occurring the endothelial cells release the tissue factor which combines

with some factors we get factor 10 release produces thrombin and eventually fibrin we also have this amplification loop that's happening at the same time so we need some of these factors we need the thrombin for this all to work

so at this point we have thrombin being generated by the pathways more being created by the amplification process and that thrombin then binds to these platelet para scepters up here and that initiates cofactors assembling on the

platelets which makes them sticky causing them to adhere to the site of injury when the platelets are activated we have the adenosine diphosphate molecule or ADP that's also binding to some receptors specifically I didn't

include the p2y on this but the p2 y 12 which then eventually winds up activating this molecule down here that molecule is normally this complex I should say is normally folded over but when the platelet is activated it

unfolds and it allows the fibrinogen to bind and then that secures the platelets to each other so with the medications that we run into in our in our practice one of the ones that you learned about this morning where the direct factor 10

inhibitors we typically see Xarelto and Eliquis the most in our practice and as you can see by the red stop signs there are two places that these inhibitors work here and here they bind to the thrombin while the while the drug is

circulating in the blood which essentially removes that factor Xa from the equation if we don't get thrombin we don't get a thrombus we don't have a plat no these things do have a relatively short half-life and in our

practice we do not monitor these with routine labs the direct thrombin inhibitors Pradaxa is the one that we see the most work one step further down the chain these are actually interfering with the power receptors so they bind to

those and that prevents the platelet activation and aggregation these can be monitored with a PTT although research tells us that it doesn't necessarily correlate with the actual levels circulating in the

blood and the different methods of sampling aren't consistent so this is not something that we routinely monitor with labs in our practice as well and I do have agents and clinical trials on here they were in trials I believe at

the time we started doing this research but as we learned this morning some of them are currently available and these do have a short half-life so their effect is relatively limited and they are reversible so the inhibitors that

work on this p2y twelve receptor are actually binding to that receptor and this is irreversible so this is going to affect the playlet for the life of the platelet seven to ten days and as we learned this morning there's a certain

amount of turnover happening all the time so there are always new platelets being produced so if we stop this we don't necessarily need to hold it for the entire seven to ten days but it is something that's going to take a while

for the patient's body to overcome and the thing that we wanted you to note about this this is an inhibitor it's an inhibitory effect so it's not necessarily captured that accurately by lab values the platelets are still there

they just don't work as well and so you can do a platelet count but it's not going to show you how well those platelets are functioning so again this is another medication that doesn't really get captured with lab values

sorry little operator error here on the remote control so the Cox inhibitors aspirin is the one that we're probably most familiar with same kind of thing aspirin is permanently affecting the platelet over its lifespan of seven to

ten days the ibuprofen the naproxen or Aleve the effect is much more limited for these medications so we're going to hold these again these are medication that will not necessarily be accurately reflected by a lab value so in our

practice we rely on oral confirmation of the last dose we literally ask the patient when was your last dose of advil when was your last dose of aspirin and we can compare it to our procedural guidelines

we also talked about these a little bit this morning we have the vitamin K antagonists warfarin is the one that you hear about you also hear about it called to mannan by the other name the liver is producing these clotting factors which

are reliant on a reaction that happens with vitamin K these things actually work by interfering with the vitamin K cycle now if you put more vitamin K in this reaction can still happen or if we add FFP that already has these factors

in it the patient has the ability to clot so this is reversible we can also choose to not reverse patients that are on warfarin Nikhil talked a little bit about the bridging that we sometimes do with patients that are on warfarin but

this is one that we still encounter pretty frequently and typically it is monitored with the pt/inr and we are currently screening for angiogenesis inhibitors in our practice these are used to treat different kinds of cancer

the one that we are primarily concerned with is the imbruvica the mechanism of action how this causes bleeding isn't fully understood but it's thought that since these inhibit the development of endothelial cells those cells aren't

available to release the factors needed to start the clotting cascade and especially if these are used in conjunction with anti platelets or anticoagulation they can really have a it can really have an effect on the

patient's bleeding risk and they can also cause thrombocytopenia thank you

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

guidelines so what I did when I created these was try to really simplify them Terry and I have given all this information to our staff nurses we've

this was a two and a half year project we took in feedback from our radiologists obviously went on off of their clinical best practice and their clinical experience this table here is a table for our low-risk bleeding

procedures I've already given you the list but within our guidelines I've created hot links where they can just click on whatever procedure they're doing in it it'll bring them to the appropriate table but as you can see for

our lowest bleeding procedures we currently we are no longer really gathering much from our patients we've deemed that it is safe for these patients to have this procedure this is also in the journal article so I would

recommend that you guys read that here's our moderate to high risk procedure again like I shared earlier we've decided to combine moderate to high risk versus having two separate tables so this one is where we also need to take

into consideration our patients and their disease processes and why they're on certain medications but this allows for our nurses to look at this list for these patients and determine how we triage this patient next it allows for

these pre procedure phone calls and our pre procedure screenings assessments that we're doing to be more expedited

now let's look at non-invasive ventilation and I know about like five

percent of the patient population that you are seeing is on some form of non-invasive whether they're on by level ventilation or continuous positive airway pressures right so see if HAP using to stent the Airways open and

maintain a pro a Peyton airway and improving oxygenation but BiPAP and patients that need co2 elimination right need help with the by level support so there's a lot of questions that come up when we give

these talks I'm like how does capnography work effectively with these different technologies of non-invasive ventilation and especially because more and more of our patients are requiring these so we're gonna look at some of the

comparisons of co2 capnography data from three different sample sites and remember I showed you that picture so that picture I showed you with the patient wearing the sampling line with a nasal oral scoop and then there was the

mask sampling port and then there was the port on the ventilator circuit distally so that's what we're looking at here so the diamonds that go I wish I had a pointer I don't have a laser pointer I'm sorry but across the top the

diamonds represent our end tidal capnography values from one liter all the way up to eight liters so as the props are as the pressures go up for CPAP they were monitoring leak rates and what they found is the cat nog rafi

values across all of those were pretty accurate when we're monitoring right here the squares and the diamonds represent the mask sampling port and the the ventilator in the circuit distal to the mask and as you could see that

quality of our monitoring goes down as we progress okay to use yes but just know the limitations of your equipment right and again this is the same thing for our BiPAP Dave data are by level ventilation we're seeing again

across the top if we're sampling right at the airway we have pretty consistent readings but then they start to fall off and we look at the other devices that are further down the downstream what we're seeing here is our end tidal

measurements again with CPAP data and what we're looking at is the patient leak so there's always leaks right when we have these devices on and that's a question well sue if I have a leak how accurate am i okay so now the red is our

nasal oral scoop and if you look at the red graph all the way across depending on the leak rate pretty consistent values right the charcoal color is the mask sampling port and that's pretty consistent probably until about like 10

right until our patient like leak rate 10 liters per minute coming out of that mast and then that value starts to fall off and even more so even further distal down our circuit when we're sampling from the circuit at the past the mask

that's the cream color pretty accurate when there's a minimal leak but as the leak goes up that falls off pretty significantly and the same holds true for our by level ventilation pretty similar distribution here with the

patient leak and the sampling so when we're using non-invasive ventilation yes it's accurate and yes it's accurate we're using high flows and yes it's accurate if we have a huge leak only if we're sampling right where the patient

is exhaling so now I hope that clears that up with the patients that are getting supplemental pressure support with your sampling and you know in those just whatever it can sample from the mouth and the nose right at the source

of exhalation has proven to be the most reliable out of all of the different sampling devices so third evaluate your

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

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

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

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

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

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

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

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

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

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

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

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

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

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

kind of the embolic protection because I think with carotid artery stenting the stents there's a lot of different types they're all self expanding for the most

part and there's not a lot to talk about there but there is with regards to embolic protection and there so there's distal and violent protection where you have this where that blue little sheath in the common carotid artery you got a

wire through the ica stenosis and a little basket or filter distally before you put the stent in early on they used to think oh maybe we'll do distal balloon occlusion put a balloon up distally do your intervention aspirate

whatever collects behind the balloon and then take the balloon down not so ideal because you never really asked for it a hundred percent of the debris and then whatever whenever you deflate the balloon it goes back it goes up to the

brain you still have some embolic phenomenon in the cerebral vascular churn and then there's this newer concept of proximal protection where you use either flow reversal reverse the blood flow in the cerebral circulation

or you actually cause a stagnant column of blood in the ica so you can't get you don't get anything that embolize is up distally but you have this stagnant column the debris collects there you aspirate that actively before you take

down the balloons that are in position in the X carotids and common carotid artery and then you take everything out so let's walk through each of these if you really wanted to pick out the perfect embolic

protection device it's got to be relatively easy to use it's got to be stable in position so it's not moving up and down and causing injury to the vessel but even while it's in place cerebral perfusion is maintained so that

balloon the distal balloon not a great idea because you're cutting off all the blood flow to the brain you might stop something from embolizing up distally but in the process of doing that you may patient may not tolerate that you want

complete protection during all aspects of the procedure so when we place a filter as you'll see just crossing the lesion with the initial filter can cause a distal embolus so that's a problem you want to be able to use your guide wire

choice as many of you know when we go through peripheral vasculature there's your go-to wires but it doesn't always work every time with that one go-to wire so you want to be able to pick the wire that you want to use or

change it up if needed for different lesions so if you get to use your wire of choice then then that's gonna be a better system than something that's man deter and then if you have a hard time using that wire to get across the lesion

you have a problem overall and then ultimately where do you land that protection device and a few diagrams here to help illustrate this generally speaking these distal embolic protection these filters that go beyond

the lesion have been used for quite a while and are relatively safe you can see them pretty easily and geographically they have little markers on them that signify if they're open or closed and we look for that overall and

blood flows through them it's just a little sieve a little basket that collects really tiny particles micrometers in size but allows blood flow to pass through it so you're not actually causing any cessation of blood

flow to the brain but you are protecting yourself from that embolic debris and it's generally well tolerated overall we had really good results in fact when not using this device there's a lot of strokes that were occurring in use of

this device dramatic reduction so a significant improvement in this procedural area by utilization of embolic protection however distal embolic protection or filter devices are not a perfect APD as you as you may know

those of you have been involved in carotid stenting there is no cerebral protection when you cross the lesion if you have a curlicue internal carotid artery this filter doesn't sit right and and ultimately may not cause

good protection or actually capture everything that breaks off the plaque and it can be difficult to deliver in those really tortuous internal carotid arteries so ultimately you can cross the lesion but you may not get this filter

up if you don't get the filter up you can't put the stent then ultimately you're out of luck so you gotta have a different option filters may not provide complete cerebral protection if they're not fully opposed and again it does

allow passage of really tiny particles right so your blood cells have to be able to pass but even though it's less than about a hundred microns may be significant enough to cause a significant stroke if it goes to the

right basket of territory so it's not perfect protection and then if you have so much debris you can actually overload the filter fill it up in tile and entirely and then you have a point where when you capture the filter there's some

residual debris that's never fully captured either so these are concerns and then ultimately with that filter in place you can cause a vessel dissection when you try to remove it or if it's bouncing up and down without good

stability you can cause spasm to the vessel as well and so these are the things that we look for frequently because we want to make sure that ultimately if we just sent the lesion but we don't believe the vessel distal

to it intact and we're going to have a problem so here's some kind of illustrated diagrams for this here's a sheath in the common carotid artery you see your plaque lesion in the internal carotid artery and you're trying to

cross this with that filter device that's what's the picture on the right but as you're crossing that lesion you're you're liberating a little plaque or debris which you see here and during that period of time until the filters in

place you're not protected so all that debris is going up to the brain so there's that first part of the procedure where you're not protected that's one of the pitfalls or concerns particularly with very stenotic lesions or friable

lesions like this where you're not protected until that filters in place that first step you never are protected in placement of a filter here's an example where you have a torturous internal carotid artery so you see this

real kink these are kinds of carotid internal carotid arteries that we can see and if you place that filter in that bend that you can see right at the bend there the bottom part the undersurface of the carotid doesn't have good wall

my position of the filter so debris can can slip past the filter on the under under surface of this which is a real phenomenon and you can see that you can say well what if we oversize the filter if you oversize the filter then it then

it just oval eyes Azure or it crimps and in folds on itself so you really have to size this to the specific vessel that you plan to target it in but just the the physics of this it's it's a tube think about a balloon a balloon doesn't

conform to this it tries to straighten everything out this isn't going to straighten the vessel out so it doesn't fully conform on the full end of the filter and you have incomplete a position and therefore

incomplete filtration so this is another failure mode I mentioned before what if it gets overloaded so here's a diagram where you have all this debris coming up it's filling up the really tiny tiny particles go past it because this little

micro sieve allows really small particles to go distal but approximately it's overloaded so now you get all this debris in there you place your stent you take your retrieval filter or catheter to take this filter out and all that

stuff that's sitting between the overloaded filter and your stent then gets liberated and goes up to the brain so you got to worry about that as well I mentioned this scenario that it builds up so much so that you can't get all the

debris out and ultimately you lose some and then when the filter is full and debris particles that are suspended near the stent or if you put that filter too close to the edge of the stent you run into problems where it may catch the

stent overall and you have all of this debris and it looks small and you don't really see it and geographically obviously but ultimately is when you do a stroke assessment and it's not always devastating strokes but mild symptoms

where he had a stroke neurologist and the crest trial or most of the more recent clinical trials we actually evaluate a patient and notice that they had small maybe sub sub clinical or mild strokes that were noted they weren't

perhaps devastating strokes but they had things that caused some degree of disability so not insignificant here's a case example of a carotid stent that was done this is a case out of Arizona proximal carotid

stenosis stent placed but then distal thrombus that developed in this case and had post rhombus removal after the epd was removed so there's thrombus overloaded the the filter you can see the filter at the very top of the center

image you can see the sort of the shadow of the embolic protection device there distally aspirated that took the filter out and then ultimately removed but you can imagine that amount of thrombus up in the brain would have been a

devastating stroke and this is what the filter looks like in real life so this is what the debris may look like so it's not this is not overloaded but that's significant debris and you can see the little film or sieve that's on the

distal part of this basket and that's what captures the debris any of that in the brain is gonna leave this patient with a residual stroke despite a successful stenting procedure so this is what we're trying to avoid so in spite

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

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

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

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