Thank you so much for the opportunity. This is a great forum to discuss these cases among interventional cardiologists. So I just want to present a case of an intermediate high-risk PE. And, you know, how we define intermediate-risk PE based on the European guidelines, those are those patients who are normal-tensive, right, but where RV dysfunction is present based on different markers. However, these patients, although they're not hypotensive, they're not in shock, they are still at increased risk of adverse outcomes. And what the literature reports is that a lot of these patients can have up to a 20% mortality in some of these cases. And it's that subset of patients who may suddenly develop hypotension, shock, and sudden death between that intermediate-risk PE that is a concern. And it's our job to identify who are these patients that may actually benefit from intervention. And those are who are intermediate high-risk PE patients. Now this case, this is a case of a 51-year-old woman with a history of knee replacement 3 weeks prior, who was brought to the ED with complaints of fatigue, shortness of breath, and multiple syncopal abysses at home. As I mentioned, she had a knee replacement 3 weeks prior and was placed on aspirin for prophylaxis for DVT. Non-smoker, no family history of VTE. And these are her vitals in the emergency room. She appears lethargic and with cyanotic lips. She does not look well. That's how the ED is calling her. She doesn't look well. Her heart rate is in between 120s to 130s. She's normal tensive with a blood pressure 110s and over 60. But she sat in 70%. They had to put her on a non-rebreather 50 meters in order to get her oxygen saturation in a balanced level. In terms of her labs, her high sensitivity to bone is high, BMP is high, and her lactate is 3.5. Now I'm going to stop there first because a lot of what… …in terms of the management of patients with intermediate VTE is about risk stratification and identifying who are those patients who are at that high risk spectrum. So I'm going to ask the panel first, how would you risk stratify this patient? Like what tools do you use? What can you consider in order to risk stratify this patient? There's so many tools out there, and I think Sandeep in the last session sort of kept it pretty simple. I like to look at biomarkers, their vital signs, their basic blood pressure, their heart rate, oxygen saturation, and how they look. We can obviously plug them into a variety of calculators, but I think we would all feel fairly comfortable saying this is a pretty classic intermediate high-risk PE patient. Jay, Tamam, any comments? I think it's exactly what you see. The biomarkers, the oxygen saturation, the clinical presentation, and definitely the imaging will help also in stratifying the patient. Anyone in the audience feel differently? Good, and which factors do you guys would consider elevate her risk? What makes her more high-risk? There's a couple of things that we consider in terms of her presentation. She presented with multiple syncopal apexes at home, that's what her family described. Altermental status. She looks disaltered. She's not able to actually complete any sentences. She doesn't look well. Tachycardia, heart rate of 120s to 130s. Her high oxygen requirement, elevated troponins and BMP, as well as her elevated lactate. So those are the factors. And just in her clinical presentation, we haven't even looked at her imaging, and those are all factors that reflect the higher risk in her case. And there are multiple calculators that we've talked about before. That includes from the PESI, simplified PESI score. And in her case, you know, looking at her heart rate, looking at her altermental status, her oxygen saturation. And even if we look at, for example, the BOBO score, that also includes cardiotroponin, the presence of RV dysfunction, as well as the FAST score. That includes not only the heart rate, also the presence of syncope and elevated troponins to identify those who are intermediate high-risk patients. In her case, if we calculate her score, she would actually be considered a very high-risk to a high-risk patient based on the scores. Now, go to her imaging. You can see that she's pretty, pretty high. Pretty significant clot burden. You know, pretty obscene amount of clot in her left side specifically. But again, it's not just about—we're just trying to make sense of her presentation. Can we attribute all of this to the PE presentation? Is there something else going on? Especially when we're in the COVID era, where a lot of the patients had high oxygen saturations just mainly due to lung disease. In addition to that, she had a pretty RV to LD ratio of 1.2. And also, she had web-shaped defects that were consistent with pulmonary infarcts as well. If we look at her echo, evidence of RV dysfunction, dilated RV with McConnell sign, and deviated septum as well. Now, I ask again, how would you re-stratify this patient and which factors elevate her risk? Anyone feel differently? Would anyone re-classify this patient? Do we still think that it's an intermediate high-risk patient, it's an intermediate low-risk? What do we think? How many people think here that it's an intermediate low-risk patient? How many think that it's an intermediate high-risk patient? Good, thank you. Okay, so basically, and what's the major concern? So the oxygen saturation, she's normal-tensive. Her blood pressure is good. The main concern in her case, to me, was her oxygen saturation and her tachycardia in her case. In addition to that, the imaging findings show, with the RV-LD ratio of more than 0.9, that it's an independent predictor of adverse outcomes. And also, the echocardiographic findings of an enlarged ventricle with, you know, decreased tap C and decreased velocity of tachycardia analysis are all signs that are predictors of higher risk in PE. So what do we do in terms of management for this patient? That's where, you know, there's still some gaps in terms of evidence. What do we do in terms of, for those intermediate high-risk patients? We know we have some registry evidence about what to do with this massive, the pieces were hypotensive. But in those intermediate high-risk patients, a lot of them have been, you know, historically managed with anticoagulation alone. But that's where the PERT teams come into play in order to, in a case-by-case basis, decide which patients would benefit from higher intervention or anticoagulation alone. And this is what, you know, also backed up by guidelines. So I want to ask, you know, the panel, also the team, how would you manage this patient? So for this patient, who would do anticoagulation alone? So on clinical grounds, who thinks that this should be anticoagulation alone? Okay. Yeah, we'll get to that, Amir, in a second. Why don't we work through. Who here feels like this patient needs an intervention and would not randomize them in some trial? Some kind of catheter-based intervention should be done. Okay, so we get a couple of hands. And who here would feel this patient would be an ideal candidate for a randomized clinical trial? And we'll walk through two different clinical trials. So a lot of people think clinical trial. Who would feel comfortable randomizing this patient in a clinical trial of two different catheter-based interventions? Or thrombectomy and catheter-directed thrombolytics? Who would feel comfortable randomizing this patient to anticoagulation alone versus some kind of catheter-based intervention? Good. So a reasonable number of folks agree that this patient potentially would be a good candidate for some type of randomized clinical trial. Very different patient, though, Amir, as you pointed out, than the first patient, in my opinion. They're all in the same category, technically. So in her case, we did decide, you know, the multidisciplinary decision was to actually take her for intervention. And if we look at her hemodynamics, and, you know, she was requiring pre-procedure, 15 liters of non-rebreather, heart rate was in the 120s, PA pressures were pretty high with a mean PA pressure of 43, and a cardiac output of 2 and a cardiac index of 1. You know, so although her blood pressure was maintained, she was truly in shock. And, you know, we did catheter-directed thrombectomy in her case. And intra-procedure, we see, you know, improvement in her oxygen saturation, her PA pressures, as well as a cardiac output and index. And post-procedure, the day after the procedure, she had improved artery size and function. As we can see, she was distressed on post-op day three on a PIXIVAN, off oxygen, and one month follow-up echo. She has normal artery size and function. Jelinka, how did you all decide to take this approach to treatment? That's a good question. So in our PERT team, we actually have—it's multidisciplinary. We have vascular medicine, pulmonary and critical care, and interventional cardiology. And basically, what we do, we take everyone's opinions in terms of what should be in her management. In her case, the fact that she was requiring—there were major factors that included that she was higher risk and that she would benefit from intervention in order to get a better recovery, a prompt recovery. And that included her high oxygen requirement, her elevated lactate, and her tachycardia. Those were signs to us that we would change her outcome. We would change her immediate outcome in terms of her vital signs, in terms of her recovery, and in terms of being able to get out of the ICU over the next day by having an intervention early. So one of the—it shows a lot about how, you know, either how decompensated they are, how the RV is maintaining the pressure. And one of the risk stratification tools, the FAST tool, actually uses syncope as a marker for higher risk. And it shows a sign of somebody who is unstable, at least for a period of time. And that's what—it's actually a predictor about outcomes in that study population from Europe. So can the panel talk a little bit about—so I think both these cases are cases of normal intensive shock, right? So the adrenal axis is compensating for a patient who's clearly in cardiogenic shock once you look at the invasive hemodynamics. And I know you've all published on that. So can—you know, part of the problem while these patients fit in that risk category, we're randomizing them, is that maybe our risk stratification tools are off. Maybe they shouldn't be in that intermediate risk category. So can you guys talk about how we can—different ways we can improve our risk stratification up front so maybe these patients aren't even being randomized because they're not—don't deserve to be in that category? The controversy there—and first of all, give credit to Samir. Samir's written one of the seminal papers on this that demonstrated that, you know, 40 percent of patients in intermediate-risk PE treated at Penn or Pitt, where he was before, you know, had indices of less than 2.1. So it's a key manuscript to take a look at. But the caveat there is that means that's what's happening out there in the world in general in intermediate-risk PE, is lots of these patients—you know, we're goalpost shifting without producing the evidence, is what I would argue. It's true that we have a deeper understanding that these patients are low output, but it doesn't necessarily mean that we're changing mortality or long-term outcomes, at least, by treating them with something more than anticoagulation alone. We really have to prove that. I think we're all confident that we can make them feel better faster. I think there is a fair amount of evidence to suggest that with aggressive therapies, but is that good enough to justify the therapies if you're not having an intermediate, long-term benefit or mortality benefit? And the problem here, when we're shifting this goalpost to say, now it's about my cardiac index on a right heart cath, and now the patient—I think the patient's massive, is it's just not what all the evidence that there, in terms of epidemiologically, has been based on. So those risk stratifications are there based on tens of thousands of patients that look that way. So I know we want to do that because we kind of feel like we know what we're doing in the cath lab, but we're going to cut off our nose to spite our faith. I know it won't affect guidelines, which means that you won't affect the population if you're not randomizing, and payers won't pay for it. Remember that down the line, too. So you're going to run into a lot of problems if we don't produce the evidence we need.

intermediate high-risk pulmonary embolism

European guidelines

risk stratification tools

anticoagulation

catheter-based intervention