Good morning. I have 7.15 on my watch, so I'm going to go ahead and get started, because we hope this will be a fun discussion with a lot of sharing of ideas. My name is Lisa Moores. I'm a professor of medicine and the associate dean for assessment at the Uniformed Services University, the F. Edward Hebert School of Medicine in Washington, DC. And I have the distinct pleasure of moderating today a discussion with four real experts in the field, and I'd like to introduce them to you. I'm just going to go in alphabetical order. So first, we have Dr. Shari Brosnahan, who's an assistant professor at NYU Langone and a pulmonary and critical care medicine attending at Tisch Medical ICU, as well as works on the pulmonary service there. She's also the senior assistant program director for the fellowship at Tisch, and she obtained her master's in science and clinical investigation and has been very active in our anticoagulation guidelines and is a member of our Guidelines Oversight Committee. The thing you don't know about Shari is she is a former D1 field hockey captain, so don't get in her way. She's also sneaky funny, so I'm a little worried, but we'll see how this goes. Next, we have Dr. Bhushra Meena, who is the program director and section chief at Lenox Hill Hospital. He's also the director of the academic and faculty development program at Northern Westchester Hospital and Northwell Health, an associate professor at the Zucker School of Medicine for Hofstra Northwell, and soon actually transitioning to be the chairman of medicine and the chief of pulmonary and critical care medicine at Northern Westchester. Meena is an avid runner and still believes that he can beat his 6'3 22-year-old son. We'll see. Dr. Parth Raleigh is an associate professor and director of the Temple University PERT program, as well as the Anticoagulation Stewardship Committee. He's also director of clinical protocols for the PERT consortium. He is a prolific researcher and a co-author on our anticoagulation in patients with COVID. Parth, this I didn't know about him until recently, but apparently he gets on these food kicks, and he will only eat that thing for the next two to three weeks. Currently, that's acai, so he's in the great place for that, at least. And last but not least, Dr. Janine Vinch, who's a professor of clinical medicine in pulmonary critical care and sleep medicine at the David Geffen School of Medicine at UCLA, an academic attending, engaged in both UME and GME. She developed the UCLA Harborview PERT program. She's also an author in our chest antithrombotic guidelines. And I had no idea how much we have in common, but Janine and I are avid football fans. You don't want to be in the room with us when we're watching, unless you'd like to hear screaming at the TV. She also admits to liking country music, or loving country, as I do. That she attained through marriage. So we have a lot to share after this. All right, with that, I'm going to keep going here. These are our disclosures, and none of these are actually pertinent to what we'll be discussing today. I'm going to let you all go ahead and scan the QR code. Hopefully, you're used to this by now. This will allow you access into the audience response. We hope you will play along with us this morning. So I'll give you just a second to do that. OK. All right, so here are our objectives. I won't read those for you, but we're going to be focusing on what we think are some key questions that may come for all of us as we grapple with the management of patients, predominantly in the intermediate risk pulmonary embolism group. But we're going to span a little bit across that. So we're going to start with a case. And we have a 38-year-old, previously healthy male, who falls while he's out biking, hits his head, has a brief loss of consciousness, and suffers some lower extremity orthopedic injuries. A few days later, presents with shortness of breath and is found to have a saddle emboli on CT scanning. He has a CT of the head done, given his brief loss of consciousness, and that's normal. You can see, initially, he's requiring 5 liters per minute to obtain a O2 saturation of 96%, his heart rate is 122, and his systolic blood pressure is 100 over 64. So our first question for you is, based on this information, how would you initially categorize this patient? Is this low risk, intermediate low, intermediate high, high risk, or do you need more information to assess? We'll just see as the votes come in. And it looks like at least a majority of you would like to have some more information. And I would agree with that. I would like some more information as well. And we will move this case along and see how that moves the needle for you. I think it's reasonable, based on some of the information that I gave you, that you would put this patient in an intermediate category, whether they're low or high risk. I'm not sure we have enough information to say at this point. There's not a lot here yet, anyway, to say that this is high risk in that the patient is not hypotensive, although he is tachycardic. And I don't think that I would argue vehemently with anybody if you wanted to put him in a higher risk category. But I think more information might be helpful. Next question for you all is, if you incorporated imaging, now granted, we only gave you one slice of the CT, but based on that slice, if you incorporated that in, which of these statements really applies to you? Do you feel confident in interpreting the CT angiogram to help inform your risk stratification? Do you feel more confident in using point of care ultrasound? Or would you prefer to have a formal echocardiogram? Does it not matter to you? Or do you not use imaging in your risk assessment? Okay. Votes are slowing down. So we'll come in and this is actually what we sort of expected, nice spread across all of these options. So at this point, I'm actually going to turn it over to the panel. I'm going to start with Dr. Mina. Bushra, do you use CT beyond diagnosis in your assessment of patients with PE? First, thank you for being here and wearing my favorite shirt that I'm not allowed to wear at home. But it was good not to have a tie and a suit. YA would be my favorite answer. I think it's, looking at the CTA, I think as we all now established that the CT scan is the gold standard to diagnose PE. But it was a, it's kind of more, if I ask the audience here, when you get the call from the ER for the PERT team and you ask about the echo or you get all the information about the blood work and the CT scan and we're going down. I think it's the CAV scan now with all our understanding, what we see in the CAV scan, we can get a lot of information, not about the diagnosis, but also risk of stratification, which is basically, well, you know, tell you what is the next step to do. I think the CAV scan can give you a lot of information about the burden of the clot, the distribution, was it lobar, segmental? And there's a lot of information you can get about looking. There's any other comorbidities, which is also can increase your risk of stratification of the patient pulmonary fibrosis. Does it have any lung nodules, suspicion of malignancy? But the main thing is when you look at, can give you even idea about the mortality. When you look at the RVLV ratio, and now if anybody involved in some of their current trials, you can see, we're not just looking at is the RVLV more than .9. We actually, our radiologists measure it now as a 1.2, 1.3, because a lot of data now tells you that all cause mortality is about two and a half fold when the RVLV ratio more than .9, even 1.3. Every one millimeter increase in size can be mortality. But also other data we can get, you know, I think is still not in the guidelines, but what we're paying a lot of attention is basically what is the staccardic output? When I see there's a reflux of contrast back in the hepatic circulation, I worry about pulmonary hypertension. I worry about this, that heart, right heart is not able to pump through. Also, we pay attention to the ventricle. If the ventricle is bowed or not, that gives you, you know, idea about, you know, where's the right ventricle volume is going to be, and whether, what are you going to be next step if you're dealing with right heart failure or not. So I think the CAT scan give you diagnosis, differential diagnosis. Part of the risk stratification as outlined in the European Society of Cardiology, if it's intermediate high or high risk, definitely there. If it's intermediate low, either right ventricle dilatation or the troponin, one of them. So really it's in the standard guideline, and whether there's going to be modified now to get more information as we understand, as more information we can get from the CT scan. That it's important, gives you risk stratification, can give you an idea about the mortality, and also can give you an idea, are we dealing with acute on top of chronic? And this is really something we are struggling with. I mean, this person can give you short, but we experience, I mean, the last time a patient we had before I came, it's been short of breath for three months, and suddenly it just had to come in, but now it's getting worse. And care scan can give us idea, this is acute on top of chronic, because also, not just what you're going to do, is the risk and mortality and the follow-up, and sometimes, well, is this kind of intervention better than the other? If there's something you're going to intervene, catheter-derated lytics, catheter-derated thrombectomy, but there's a lot of information about chronicity of this clot, whether it's in the clot itself, is it a complete occlusion with some pouches, whether this is extrinsic, if this is stenotic or post-stenotic dilatation, if the right ventricle is thick or not, mosaic appearance, all this kind of more information that I'd be happy to decide what is the next step, you know, at this point. Great. I'm going to let Parth maybe argue with you a little bit. I think Parth is a big ultrasound fan. He's quite an expert with the probe in his hand. So what do you think, Parth? Yeah, I'm a gritty learner, so that's always my disclosure. Some of you might remember my talk yesterday. I spent 15 minutes talking about how much I love CTPA, but today is a different day and a different coffee in the hand. So I'm going to go the other way around. First of all, I just want to ask my audience, who does the point-of-care ultrasound by themselves? Okay, good. And who would have done this in this case? Or if you had a probe in your hand, would you put a probe on this patient before you go forward? Great. Also, I saw also another question I wanted to ask before, that they said this patient had some time. Who would have done a venous runoff on this patient while you are doing CTPA, provided that you are called on time? Anyone? Okay, someone. Yeah, so I think point-of-care ultrasound, I would have definitely put a probe. Some of the observations that I would like to make on this, obviously, we didn't show you, we give you a blood pressure of 100 and heart rate of 122. We did not tell you what the baseline blood pressure is. So one of the first thing that I probably would approach is like go back in the chart and see if they have any previous history of what even an outpatient visit, what that normal blood pressure is, right? So those 14% who said it's high risk, maybe the baseline blood pressure runs around 160. So drop in systolic blood pressure, 40 millimeter mercury, could have been, we may be dealing with a massive clot. This patient had a lot of orthopedic injuries, right? So who knows that this patient is not a little bit hypovolemic, right? So CTPA is not gonna tell you whether a patient's volume status is, right? I think, Meena, I think we'll do that, and they published that recently, knowing that what is happening in the leg is the second part of the story that we need to figure it out. I think the clot we saw was saddle, obviously, clot itself may not tell you anything, but I think the story does not end. It's a continuum of spectrum. So I think what's happening in the leg is equally important for me before I jump in the conclusion. So I think I would have done an echo. I think if this patient, what if the IVC is completely collapsible, right? What if there is no TR on this patient? I think you would be okay to give small boluses of fluid, and I think whether we like it or not, we always talk about that you can give fluids, you can give fluids, but trust me, a lot of patients, before we called by the PERT or ER, ER always have boluses, and not all of them have collapsed from a dead RV failure. So time and again, yes, if I see a completely collapsible IVC and somebody's hyperdynamic, we have in fluids to stabilize them. So, and that only echo, I mean, CTPA will never will tell you that. So I think that's the thing that I would definitely vouch for an echo in this case. Second, CTPA does not pick up the clot in transit, right? And again, where you treat clot in transit is a different story, right? But picking up a clot in transit to somebody who has a settled clot like this adds to the story. So I think doing a DVT study, doing an IVC, I mean, looking at the IVC collapsibility, looking at clot in transit is important, right? Maybe this was a massive PE and there's a functional PFO. I mean, you may be thinking about your out, right? So a lot of 10% of PE, a lot of populations will have PFO 10% time, but maybe that PFO opens up when the right heart is in the strain. To your benefit or your disadvantage, you don't know that, right? I mean, many times you'll see a patient present with a stroke and they have a PE and it's a PFO which is kind of doing that. So I think those are the four things, particularly in this case where I don't have a good sense what I'm gonna do and this is kind of a sicker kind of patient. I would argue that these are the basic point of chiral-to-sound views. I'll not put my chiral-care echo board certified head where I go more and do some extra crazy measurements. Any cardiologists in the room by here? A few, okay, so yes. So I think that was the most humbling experience I had. So taking in a chiral-care echo boards, how much I respect my cardiologists. Before I did that, I thought they read the echoes the way I did the PFTs, we just make something out of it. But now I see the other side of it. So I do respect a lot of advanced cardiac imaging. So, but yeah, I think to a point, I think Jim Horowitz and some of the NYU colleagues have also gone ahead and published the role of VTI and role of measuring the cardiac output in the acute PE setting. I think that's important. I think as Meena mentioned, that if you know how to get a good point of chiral-to-sound view and if you're gonna get a good TR jet and know the simplified Bernoulli's equation, you can start thinking about what is acute and what is chronic, right? I mean, if you think about PE 60-60 sign, again, it doesn't have to be exact 60, doesn't have to be exact 60, but I mean, these are the simple things that you can put your next step to it and identify what is acute or chronic to help your patient. So I would argue that yes, CTP is extremely helpful, but I don't know whether you need a formal echo on everyone because I think there are enough studies to show that there's formal echo versus the reporting and doing a formal echo. It takes 14, 15, 16 hours. And sometimes you don't want to wait that. So I think it's up to us that we get good with what we do. Yes, so I would say echo always, point of care echo always. All right, I'm sure our other panel must have comments, but I'm gonna pick on them for this next phase. So we're gonna give you a little follow-up. We have the same presenting information, but we also have some additional information. So we have a positive troponin. The left atrium is 2.3. The simplified PESI score is three. You can see the RVLV ratio, as Meena mentioned, is 1.1. And we did obtain an echo and saw a moderately dilated right ventricle. So what therapy would you initiate at this time, given that information? Would that be low molecular weight heparin, heparin with or without a bolus? Would you initiate therapy with a direct oral anticoagulant? Would you put in an IVC filter? Okay, so about close to 60% chose low molecular weight heparin with the rest heparin with Ebola. And we're going to come to the panel on this. I want to take a step back maybe if I could and ask Shari, if I were to have asked you that question, what would go through your head? What else would you need to know before you answered that question? So I think Parth brings up a lot of points about what I can get from the echo. So I think understanding if there's a current PFO or not. I'd want to know what time of day it was too because that can matter to what backup options I have. And I'd like to know the size of the patient, the BMI of the patient. And basically those would be my major things that I'd be concerned about. And then I love knowing if a patient has a DBT or not because this can change kind of. I always like to know the future and so be prepared if something bad happens. So I'd like to know if there could possibly be an acute bursting in the patient. So Shari, if I may ask you a question. You said BMI, why? So I have, I think that there's a lot of this choice between low molecular weight heparin and heparin is a very interesting one because I think that there's a lot of push to go to low molecular weight heparin. But the pharmacokinetics of low molecular weight heparin can be very varied in patients and I guess I need to know the creatinine clearance of this patient as well. But it depends a lot on how quickly I need to get that patient therapeutic and how effectively I think low molecular weight heparin would work in this patient. So I am a big proponent of using heparin with a very aggressive bolus strategy, especially if there's a lot of clot burden. And the reason is because on the outside of the clot there's actually antithrombin and you can have mild heparin resistance or even major heparin resistance depending on the patient. And you aren't as aware of that if you have low molecular weight heparin. I doubt many people are checking 10As in their low molecular weight heparin patients or even have a treatment strategy based on that. But I think really going hard with your heparin bolus and making sure you get that patient therapeutic very quickly and checking PTTs or 10As depending on your algorithm is extremely important. Yeah, can I pick on you because I struggle with that a lot. So who follows the 10A levels versus heparin? It's 10A levels, sir? In low molecular weight heparin? Yes. but do you do it for low molecular weight heparin? Okay. And what's your experience? I mean, do you see the data or it's still sketchy? Because somebody just, some very literate person showed me yesterday some of the slides on low molecular weight heparin, and it's still all over the place, as Sherry was saying, the 10A levels, we think they are therapeutic, but they are not. So is it your experience too, that 10A is also very sketchy after the dosing of low molecular weight heparin? It helps to have the 10A levels because you're not closing, how do you get to the low MSR? Can you give us an example? Just grab. I have a little something we struggle with, especially when you deal with inter-hospital transfer patients. We have two ER downtown, and coming from downtown to uptown might take half hour, even with a siren. You know, a patient given heparin, bolus, and now it's going to be maybe six or seven hours until they come to our hospital. And then PTT, either normal, or PTT, either 200. I mean, the question now, there's something we struggle, is they're undershooting or overshooting with the heparin. Is this is something we should really go with the Luvonex, especially if we're going to be transferring low molecular weight heparin, especially if we're going to be transferring a patient, and there's going to be time to draw the blood? Yeah, so Parth is definitely the expert on transporting patients with VTs, but I will say, I need to know if a patient has a DVT before they transfer with a massive PE, because I worry about that breaking off. I do think there could be some role in that case of giving a heparin bolus and then following with low molecular weight heparin, right? So you're sure that the onset is, so sorry, does someone has a question? Like, I think what choice we pick from these ones is what we would anticipate in one hour or two hours that that patient might need. So, sir, I really like the way you think. I think, in this case, I think, I mean, at least I would have agreed with Sherry to give it Heparin bolus. So, and I think this is what we want. So, please, I want our audience to speak up their mind because we want to interact. So, please, keep coming with that question. There are certainly people that will do that same approach, but they would still use low-molecular weight Heparin. So, I'm not sure thinking ahead necessarily discriminates between the two. I think that that's perfect, and one of the reasons I would choose Heparin, but I will point out what Dr. Morris is saying is that low-molecular weight Heparin does not preclude me from doing any of the rescue strategies that I would do, including catheter-directed thrombolysis, catheter-directed therapy, or TPA. I would feel comfortable giving that if I needed to give that to this patient. I assure you, but you said you feel comfortable, but when you give TPA with Heparin, don't we stop Heparin? And then you actually check PTT two hours after, and then PTT is in whatever magic numbers, then we start. So, I think, don't you think that that patient should be, this patient, if it's massive, should have been just on Heparin bolus because low-molecular weight is not gonna go away knowing, hoping that it's all therapeutic. Maybe we'll let Tim have a comment. So, a minor comment is the anti-TENU level is actually geared towards low-molecular weight Heparin. Low-molecular weight Heparin is an anti-TENA activity. Heparin is a thrombin, anti-thrombin agent and an anti-TENA agent. And so, doing a test that's geared towards low-molecular weight Heparin may make it look like low-molecular weight Heparin is just a little bit better as far as its pharmacokinetic profile. In addition, we really never established what a real therapeutic level is of anti-TENA for low-molecular weight Heparin. That wasn't part of all the trials that registered things. So, I would be a little bit cautious about saying, it's automatically right if you give low-molecular weight Heparin and not if you give Heparin. And one other just minor consideration is that if you were to go to an embolectomy or something, remember, those are big, giant, fat catheters and those things have to be kept clear of clots. And so, you have to give lots and lots of Heparin. You have to give a ton of it, so much so that you're using ACT levels to follow the Heparin levels. Those are based on antithrombin activity. So, the low-molecular weight Heparin may actually hide a little bit of the anticoagulation if you're choosing to go for a catheter-based therapy. Completely agree. And then, I think the point that you're making is also that the TENA levels vary between goals for unfractionated Heparin and low-molecular weight Heparin. And so, they're different goals. You can follow them for low-molecular weight Heparin, but I don't think it's a one-size-fits-all dosing strategy, one milligram per kilogram, which is what we think makes people therapeutic. It does not always. And I think, Dr. Morris' point, I think I don't know the exact mechanism, but when you do Heparin PTT or TENA, it's not actually Heparin levels that we are measuring. So, there's no, I think there's some antibody that doesn't allow us to measure the Heparin levels, is my understanding. So, it doesn't exist, so you're measuring indirect measurements of exactly what you're experiencing. So, we'll do one more comment on this and then... Couple of comments. One was... You're allowed all... No, no, just one. Okay, the first one regarding this stuff, I agree with you. We almost never use an Oxoparin in this situation for all the reasons everyone just mentioned. We're reliant heavily on TENA levels at our institution and in our system in general, through five or six hospitals. What we do for ECMO circuits, for submassive PEs, for symptomatic risk, et cetera, is IV Heparin with or without lytics or intervention. I agree with you for using NARI catheters, it's one thing, but if you're doing an angiovac on a clot-in-transit, it's a whole different ballgame. But, you know, the bigger comment I had was brought up earlier. You know, we've gotten away from using systolic blood pressure or mean arterial pressure as a criteria for shock completely. If we're seeing lactic acidosis, if we're seeing any evidence of endorphin dysfunction, to me, as a clinician, that's massive P. And I struggle with not giving these people systemic lytics up the gate. So would you like to comment on that? I'm gonna ask Dr. Vinge to do that because we were talking a little bit about how, as a group, how important other biomarkers are. And I think your point about blood pressure is an excellent one, particularly since we don't know the baseline blood pressure of this patient. So this could be significantly hypotensive. So even with that, I wouldn't even necessarily need these other things. But they all add up, right? And they all begin to paint a picture. So Dr. Vinge? So I was trying to decide if I wanted to further look at the bleeding risk first because I still don't think we have all the data on this individual yet, as well as you already started some of the discussion about what other data do I need to have to move this patient forward and decide what's next? So we have the troponin here. The BNP is also an important measure. I get the chemistry, and on the chemistry, we have a lot of data. There's some information that hyponatremia is actually associated with in-hospital mortality. So if they're hyponatremic, that might make me a little bit more nervous about the individual. The creatinine clearance, whether I calculate that, whether I look at my serum creatinine, whether I get a cystatin C, or some of the other labs to look at renal function, is also a predictor not only of bleeding, but also has been associated with outcome. The lactic acid, acidosis, is also becoming an important marker. And we do know that some of these patients, there's recent data from the flash registry that Boucher was a part of that just reported on these subclinical patients with shock, where they're normotensive. They look outwardly like they're doing OK. But if we look at other end organ perfusion, if we looked at their cardiac index, as they did in the flash registry, you actually find that a proportion of these patients are actually not doing as well internally as they may look like they're doing externally. So having additional data and recognizing that we can have patients in subclinical shock who are normotensive, and maybe, again, that patient that we're going to be worried about, about offering some form of advanced therapy. Now, we also have to go back and say, well, this gentleman had a fall and hit his head. Is this someone that we really are going to want to push lytics on? Or are we a little bit worried about that injury and may want to do an advanced catheter-directed intervention instead? And so really trying to go back to the bedside, getting the data about the DVT. I like the hemodynamics as well. Heart rates, for me, are also on the scale of things that make me very anxious. The patient with a heart rate of 140 is a much scarier patient to me than the patient with a heart rate of 90 to 100. And we have data that as the heart rate goes up, the adverse outcomes from that patient in the setting of an acute PE is also important. So while we look at the clot burden and we look at the echo, I think there's vital signs and laboratory data that also supplement that information so that we can really have a full picture as we're standing at the foot of the bed. So I think the other important thing is never walk away from the bedside. Always keep going back to the bedside and see what your patient's doing over time. You may start your HEPR now or your low molecular weight HEPR now, but if in an hour from now, they're much more tachycardic, you've got all this data now, you're going to move them forward likely to another intervention in order to help stabilize them. The other thing I like to do is, as a lot of you have pointed out, is planning ahead. As we do our PERT team, I'm like, make contingency plans. While the patient looks fine in the moment, they may not be fine in two hours from now. And I don't want to get that call at 2 in the morning and then try to go through my lytics checklist. So I have what I call my lytics checklist. So up front, when we see the patient, we're like, in addition to bleeding risk scores and trying to decide where they're at from a bleeding risk standpoint, whether they're low, intermediate, or high risk for bleeding, it doesn't mean I'm going to stop them from getting anticoagulation. It just means I'm going to prepare in advance for possible bleeding events, meaning I'll type and screen them. I'll put two large IVs in them. I'll put them in a higher monitored setting. And I'll just be prepared, and I'll watch hemoglobins maybe much more closely so that I'm not stopping them from getting the treatment they need for their disease, but I'm going to watch them and try to resuscitate them more early if I start to catch a bleeding complication. And then as getting to the lytic piece, I have a checklist that we just go through and say, if this patient deteriorates, I know in advance that they either have a contraindication for lytics, and my next step's going to be catheter-based, and I've got my cardiologist or my radiologist on board and ready to go, or they're a lytic candidate, and then I'm going to take care of them in my ICU with lytic therapy. We cheat when we get to the bleeding risk. So in our notes, we have two, and we take the highest risk. So you mentioned, which is the best bleeding risk score we can use at this point? Or if there's any agreement of which one we can just offer? Should we poll the audience? Parth, do you want to ask? Say it again. Yeah. Let's see what people are doing. Yeah, anybody can shout out their favorite bleeding risk, or if there is a risk. There are so many. Or we could go through them. Say it again. BACS. BACS is your favorite? OK, BACS. So BACS was published by Dr. Davis and his group. It's the only validated, derived respectively, prospective validated in the VT command registry and involves four parameters. And it actually predicts the major bleeding in the patients who are getting TPA. So that's a BACS bleeding score. Any other fans? Well, I have a simple answer. What is that? that we're trying to do, you know, by tying ourselves with so many burdens that we're using systemic PE. And I still don't understand, you know, what you have. It's end of PE. You have blockage to 78% of people who would imagine that all the implications on your life are capped. Why did you even create this paper? It's so difficult to cover. Well, certainly, I would argue that part of it is in the long-term care of PE. So not necessarily pertinent to right here. It is very important long-term, particularly in determining duration of therapy. But up front, I think, to Dr. Vinch's point, it may not stop you, and it probably shouldn't stop you from doing what the patient needs, but you're going to be ready for them to bleed, and you're going to have things ready to go. And I think it's helpful in that instance. I think it's a different beast, though, a little bit, because it depends on what the patient is about to lose, right? If the patient's going to lose half their brain because they have a stroke, then giving the TPA is different than if I think that I might be able to support the patient with either a catheter-directed thrombectomy, or if the patient is coding from a PE, right? If the patient, then I think that giving thrombolytics, no matter what, there's no downside. But if the patient's the cure, I'm not convinced that you're going to have to do anything to support him young, healthy. Heart rate's 120, lactate, but I've seen patients who have been okay. And we have other options. I could put this patient on ECMO, right? Like, I have other things I could do that don't involve if I think the patient might bleed in their brain. Truthfully, the oxygen makes me nervous, right? It means that maybe there's a PFO, and the idea that something went across makes me a little bit nervous that the stroke risk is a little higher. So I think it really does depend. If someone is going to have a massive heart attack that's not going to reverse, someone's going to have a massive stroke that's not going to reverse, I think that's different than someone who I might be able to support with other things. We haven't given them INO. I haven't given them dopamine. I haven't done anything that I could, and I'm not saying those are standard treatments for PE, but I also don't want to make someone bleed into their brain when they could survive it with little consequence. You know, I would say that there is a difference between a stroke and an MI and a PE. In a stroke, the brain cells are dying. They're not at risk for dying. They are dying. In an MI, the cardiac cells are dying. In a PE, what you're afraid of is the next thing that's happening, and what this patient, what you're describing this patient, most patients that are like this do fine. They get anticoagulated, they do fine. The heart isn't dying. Stuff isn't dying anywhere. What you're afraid of is what's going to happen next, and I'll ask the question that I ask in all these presentations. What do you think is that's going to happen next? I mean, do you think the heart's just like, it's going to beat for a while, and then it's going to get tired of beating, it's going to stop? Or is this a recurrence? Or is this, I mean, we know about recurrences, right? 10% of people in this situation have a recurrence within the first week, or, you know, the embolization of the DVT, you know? So, I mean, something, we're all worried about something else going to happen, but the big question is, physiologically, what is it? I think that's my... Comment in the back first, and then, and then, please. Sorry, I take your comments after that. You, yeah. I'm just curious, in terms, because many of our patients that have PE have underlying cancer, not in this case, of course, and your patient's coming in, you may not know the extent of their cancer history, or it's not completely staged. Do any of the bleeding risk scores take that into account? Because you don't want to give TPA to the patient who has, you know, micromets in their brain, and then has a massive hemorrhage. Several of the risk scores do take that to account, but they don't actually specify the specific cancers. So there are some cancers that, in my mind, make me completely nervous about things, like, I think, sorry, just a melanoma in my ear. So that's one that comes to mind that just really is a bad player, that when I've seen them bleed on just heparin, that I wouldn't go down that route. So they do include cancer on several of these bleeding risk scores, but they don't actually go down to the exact cancer type, which I think is also important to know. And there are specific scores developed in patients with cancer, but not necessarily in this acute setting, unfortunately. So I usually treat STEMIs mostly. I'm a cardiologist, and this patient, who had not good lytics, who, you know, fell on the ground. That's basically, you don't apply any risk score. I gave tons of lytics to patients when I was a fellow, and when I called my attending, who was Julie Hockman, she said, anyone who has fell on their head is out. So you don't apply risk score. That's not a question, I think, in this case. And that goes along with the literature. Forty percent of the patients in the FLASH study had contraindications to lytics, and that can be duplicated in some other trials, some other surveys. All right. Should we move on? Okay, so a little bit more information. Again, some of the initial information. We're purposely not changing that on you. We're just adding, so now you also have the fact that the patient has bilateral proximal DVT. So you get to decide, how are we going to treat this patient? We've been tossing that around as we've been doing our risk assessment. We've been talking about additional factors that help us. We've been talking about perhaps the bleeding risk, although not specifically in this patient. Are you going to anticoagulate them? Anticoagulate with a filter? Use some of our, and I won't specify which here. I don't know that we have time to go into which catheter-based treatment. Half dose, full dose, put them on ECMO, or do you call your surgeons? Any surgeons in the audience here? One of you will have to argue in favor for them. I think this question should 100% vote. We have more than 70-67, so please vote if you are not. I don't know who you are, so. Okay. So interesting. We had about a quarter that would anticoagulate. Some of you would anticoagulate, but also put in an IVC filter. Forty percent at catheter-based treatment, and then we have a few votes for half or full dose TPA. So I want to open it to the crowd. I might ask each of my experts first. Just don't go into a lot of detail, because we'll expand, but just, I'm going to put you on the spot. So, Bhushur, what would you do? C. Okay, so you would do catheter-based. Parth? Yeah, I think I'll ask one more question. Can this patient lay flat? No questions. No questions. Actually, I made that question. I still don't get to often answer. Go ahead. No. Okay, fair enough. No. I think one of the things that will help me decide C versus this is, is this patient stable enough to move? I didn't show the, I mean, if he can lay flat, and if he can move, because a lot of patients with E can lay flat, and that takes my catheter options out. So if this patient can lay flat, I have time to transport. I'll do C. Otherwise, I may go with B. Sorry, but C and E. I'm going to be different. I'm going to go with A first. I think at this point in time, while he has some features that are concerning, I think he's young, and I still have some time to observe him. I am going to, though, make sure my radiologists and my cardiologists are available and aware, and I've gone through my checklist. I'm worried about this head funk, so I actually would sit on him with anticoagulation a little while longer, but have a contingency plan that if he decompensates further, gets more tachycardic, has other signs of hypoperfusion, then I'm going to go with C. What is C? Is it mechanical catheter-based or pharmacologic catheter-based, which is a difference to me? Yeah, I think that's a great question, and I think that's something that I make in concert with my IR or whoever's doing my intervention, depending on the hospital, what is possible, but if, you know, running the checklist and there's definitely a contraindication to TPA, that kind of brings up C in my mind, right? Like I might just do a catheter thrombectomy, but I agree. I'm still A. I tell my patients all the time when I see them, I have one point in time on you now. Until I know what the next point in time looks like, unless you've declared yourself, I don't know which trajectory we're going on. I think a lot of things make me nervous about this patient, the bilateral high DBTs, the lactate, but he's young, and if the tachycardia comes down with just a little bit of heparin, which always has a calming effect, I feel like, I would, I think we might be okay with just anticoagulation for now. Just debating each other. I think at this point, you know, A, you're going to wait for something. At this point, all the scoring system that we have is not a dynamic one. It's a point, at the point of care, it's stationary, only when the initial diagnosis, but I think if we're going to wait, what are we going to be looking for? What are the markers? What are the trends we're going to be looking for? At this point, we really don't have any standardized dynamic scores. I think one of the hypotheses is the news, which might be the future to go, but. I just use bedside watching. I mean, I watch their hemodynamics. I watch their breathing pattern. I watch their oxygenation. I watch their heart rate. Their heart rate's really key for me as to which direction they're going, as well as just moving them in bed. I might get in the room, and if they're laying there really calmly, their heart rate's 80, but if I sit them up, and they go to 120, I know they're still in trouble. And so I do a lot of my assessment at the bedside when I do this watch and wait. Yes, sir? patients. So the question in my mind, what does the evidence show? If you're rolling in a trial, what's the question? I yes, go ahead. You are two steps ahead of me, so I'm two steps below, so please go ahead. No, I hear what you're saying, and I actually feel like I felt that way at times, like I have felt that. But what I have found is this patient, the amount of syncope that comes, I used to think syncope meant massive, I used to think it was totally massive, but it's not, it happens. In Europe it is, in the USA no. No, because I'm talking about a study that came out, I was not making, it was not one of those dad jokes. But if you remember the syncope. He has really bad dad jokes, actually. The amount, well no, the amount, so I think Parth is alluding, and I, maybe not as well read, but the American study said about, I forget, one in three patients with high risk submassive Ps actually have syncope, with no persistent evidence of end-organ. And in my head, when I back up what happened to this patient, there was a saddle, right, and it maybe sat higher for a second. Maybe for one minute the patient did occlude, their PVR went to a billion. And then it went down when it went forward a little bit, right? Every clot was a clot in transit, every large clot that went to both sides probably was a saddle at some point. And so I do agree with you, maybe when the patient fell off their bike because it came out of their leg, it was massive there. But this is my two points in time. I need to know if the lactate stays. If the lactate is five and now it's two and a half, then they're better, they're getting better and better. But Sherry, with PE, lactate does not go to five, they die. I mean, there is a lactate of four, it has 50% mortality. And this patient has not one marker, this patient has multiple markers, right? You take DVT as an individual with PE, four times higher risk of mortality, four times higher risk of recurrence, 90, and that, you have an AK, you have multiple markers on this patient. So I think we should not be afraid. So I think one thing I'll tell you that I completely agree, and Dr. Morse, if we can advance to that risk certification class, I think this is what you're talking about. This is not a traffic light, right? This is not red, green, and yellow, right? This is a pendulum which is moving, and I think your patient that we have right now is right in between the red and orange, and I don't think I have problems agreeing with you that this has more than one evidence of impending doom. So in our perspectives, we haven't heard, and what we would decide on is... So I want to push you a little bit on this one. I think your point is very well made. We, as a community, are talking about the limitations of our current approach to risk stratification being based predominantly on prognostic scores, right, at one point in time. And we don't follow them successively. And so I think there's a real movement towards looking at more of a, what we would say treatment-based or outcomes-based approach, which would sort of get at what you're saying, is like, what's the best treatment for this particular patient, not which box do they fall into? But my question for you would be, you're worried about giving him lytics because he hit his head. You're saying he's high risk. What data do you, can you share with us that says you're going to go to catheter, why not call your surgeon? We do have a surgeon. So this is a collaborative. I still want to go back, but what are our definitions? Because if we can't even agree on what we're defining, how the heck are we going to go around these algorithms? Because I think we put the cart before the horse. Well, I also want to bring it back to the point that was made about what the evidence is for catheter-directed therapy, right? Because I think you're saying, well, I know I'm going to get them better. I'm not sure catheter-directed therapy has been shown to be effective in massive PE. So let's go back to maybe high-risk submassive. And in that case, I know I can make the LVRD ratio better. That's all I know. That's all I know. I can fix that faster than I can fix it with other things. Maybe not fix it faster than TPA. So what I would extend is that we have a lot of registries that are sponsored by industry that are helpful to, that I know that these are relatively safe procedures, but I hope that we have an answer with P-TRACT in the future, which is a randomized clinical trial that is currently enrolling multi-center, looking at heparin versus any catheter-directed therapy, thrombectomy, thrombolysis, depending on the institution, one-to-one randomization of these high-risk patients. And I hope, and it's free from industry, and I hope that we have an answer for you in the next three to five years. As Ms. Achari is pointing out, we don't have the physiologic data to know where these patients go. We just have the echo and the CT data right now that's driving this. And I think a lot of people have been worried about what the clock looks like, we need to pull it out and they get better quickly, but we need that data to really be sure that we're doing right by them in the long-term planning, and that's what we're hoping to do. Yeah, and I think to your point, Janine, right, even these outcomes that we do know, Shari, which aren't many, are very short-term. We don't know long-term how these patients are going to do and how many of them are gonna come in with persistent symptoms. Certainly CTEF being one far extreme of that, but a whole spectrum of symptoms, and we don't know how we're impacting those either. I'm hoping, again, some of these trials will help us with that. But let's get some more comments from. I just had a question. I said one of the problems I see is when I come to these meetings a lot, I think there's a division between two different doctors. So there's ones who only treat based on clinical evidence, and there's one who are just in the real world is to say, hey, I'm seeing this patient in front of me, what's in front of me, what do I have, what can I do? And my major concern is when you see these patients with a high intermediate risk and you just wait on them, nobody tells me when they crash, they crash. So the question is when these people crash and they're, oh, I'll start LeboFed or I can start this, they may not even get to the LeboFed, they may just die. So one of my questions in the back of my mind is when I see a patient like this that that's young and you wait it, my question is what's, is there any information of when these patients crash, do you even have time to do all these things that you were thinking about? So to me personally, I would rather intervene on something so that this person does not crash and I have to do more. And if it's catheter-based treatment, which may have a low risk of bleeding, that's one thing. But the hard part about these conferences is you have the people who actually follow clinical evidence and other people just say, hey, I got this patient in front of me and I gotta do something. And it's very hard for all of us. If you've ever seen a patient die from catheter-directed therapy, I think that changes your mind. I've seen patients die from catheter-directed therapy and patients that I'm confident would have lived if I did not send them to CDT. So I think that you're kind of, you know, not in a great place if you do, not in a great place if you don't. But I don't know the answer. I know the answer is the RV will not sustain any more time, any more stress. I need to send them and I need to relieve that. But all I know is that I'm making that RV better. So what- So what's the cost of that operation? In fact, who would you say, who died? After he goes out and runs that operation? Who's cured? Yeah. So yeah, no, they died as a relationship to the sedation used for the procedure because their RV wasn't good. So I mean, I, there have been several, I mean, I don't wanna get into like, you know, bad outcomes, but CDT can have consequences. And I think the flame and flash do tell us that they're relatively safe, but there are still people with bad consequences. So I think this is a, reflects what's going on with every PRRT team. It's a real life discussion. We go through this, the same thing. But I think the intervention is where, what are your institution, what your resources? And that will decide that, for example, us, we can even activate the cath lab, even use the hybrid room. I can get the patient to the cath lab before I can get the NECO. So this is kind of more what you do for the patient is what your resources, your experience, and the ability and the support you have, that will dictate. I mean, patient like this on a bicycle, the heart rate is one. I think it's something I'm gonna be coming on about is this is like a, you know, a volcano, need to erupt, the patient's gonna crash, if you sit on him, but we don't know at this point. Your resources and experience and your backup is gonna help you to make a decision. And there's some study shows the effect of the part in the weekend versus the weekdays and the night. And this is kind of more, it's a clinical decision. And we all go through this, even for academic centers, the same thing. So just a point of clarification about the previous two questions, it actually could have been coordinated perfectly. Well, one was about, is it was the clinical evidence, and the other was about like, why don't we call these things, you know, massive or something like that. The naming that the ESC used for these PEs a little bit unfortunate, you know what I mean? A high risk patient, high risk patient is a person who got a DVT after a day after neurosurgery, that's a high risk patient. You can imagine, he's gonna bleed into his head, what do you do, that sort of thing. So those are high caliber decisions, but what the folks are trying to do is to try to group these people into groups that maybe had clinical trials where everybody was similar. So they just happened to call, you know, the massive one where you are on vasopressors, you're gonna call that high risk, and the intermediate is where you weren't, but maybe there was markers, and that puts you in a higher risk group in the intermediate and lower. What they're really trying to do is to enable us to make decisions based on the evidence. And unfortunately, in those high groups, any color, you know, darker than yellow, every study ever done was negative, you know? And so we're here, you know, kind of within the absence of data, saying what we, you know, our gut feeling is, you know, what do we think would work, and that sort of thing. And so I agree with people that are saying, like, you know, right now, a lot of this is left to our clinical judgment about what we think's going on, you know? Right, yeah, and I think your point, Tim, we talked about this a few weeks ago. We, all of us, I think, recognize at this point that that intermediate risk, which is, if you use that classification, up to 50% or more of patients coming in would be somewhere in that category, and we know they're not all the same. But we, once they kind of cross that into anything darker than orange, we say they're all the same, and they're not. And we don't know how to further address those patients. Are there ones that would fail lytic therapy? And we would call the surgeon earlier. Who needs assist devices? Who might do fine with anticoagulation, but might need ECMO to help along the way? I don't think we have the answers to those questions either. So it's actually why I love this field, is that there's still a lot we don't know, and it does involve our clinical judgment. I think that's why we all like this. For most of us, I would say, I started, when I started my training, PE was a disease that we approached by the disease state. Every DVT got treated a certain amount, or amount of time, because it was a DVT, and they got three months, and every PE got six months, because it was a PE, and that was the end of it. And we have really taken a journey towards more personalized, individualized approach to the patients, both in the acute treatment, but also in their follow-up, and in selecting patients that might benefit from extended therapy, and these are still evolving. So I think it's fascinating. We wanted to show you some of the trials that will be coming. I wanted to let you know that we are constantly updating our antithrombotic guidelines. Yes, they are evidence-based, and I understand that they don't answer every question for you, but it's our attempt to take the best evidence that we have, and try to give some guidance. So we are in the process of updating our prevention in the medical patient. We will update antithrombotic therapy again within the next couple years, and we're hoping, as we get more and more data, to tackle how we deal with patients after their acute event. I wanted to share that with you. That's just a list of resources. If you would like them, those are not all, but some of the papers we use. Those, I hope, will still be available online. You should be able to access our slides. And I want to keep us on time. We can move to the back of the room. If folks have other questions, please evaluate the session, and I want to put in a final plug that, as I said, this acute PE isn't the end of the story, so there'll be another wonderful session same time tomorrow morning, 7.15, in room 314. Dr. Morris is going to be leading a discussion on the evaluation for post-PE syndrome, so I would encourage you all to continue the journey with us tomorrow morning. Thank you very much. Thank you.

pulmonary embolism

risk stratification

treatment options

anticoagulation therapy

catheter-based treatment

thrombolytic therapy

individual characteristics

dynamic risk stratification

post-PE syndrome