Team-based Care of Pulmonary Embolism - Insight from the New Guidelines

Join our guest, Dr. Jun Li from University Hospitals of Cleveland, for a discussion of the newly released Joint Society Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Dr. Li was a co-author of these guidelines, released this past February. She reviews the clinical, laboratory, and imaging aspects of PE diagnosis, as well as the new severity classification. She then addresses management, including updated recommendations for anticoagulation, risk assessment, and the roles of both catheter-based and surgical intervention. Finally, she reviews the evolving role of the "Pulmonary Embolism Response Team" in the acute care of these patients. 

For more information, see:

2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults

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Transcript

Kanny 0:09

Welcome back to the CardioHL Podcast. This is Kenny Grewal here in Columbus, Ohio. We hope everyone's having a nice summer. And I'd like to also welcome back my co-host from Cleveland, Dr. Ellen Sabik.

Ellen 0:22

Thank you, Kenny. I am very excited for today's topic. We'll be talking about the new ACC/AHA guidelines on pulmonary embolism. And I actually have the honor of introducing my colleague, Dr. June Lee, who is an interventional cardiologist at University Hospitals Cleveland Medical Center. She's also the director of the Harrington Heart and Vascular Institute's Limb Preservation Center. And as an interventional cardiologist, in addition to coronary interventions, she's very involved in both PAD space as well as pulmonary artery intervention space. We're very happy to have June here today, particularly because she was one of the co-authors of the newest guidelines. So June, welcome to the podcast.

Jun 1:08

Thanks Ellen, thanks Kenny for having me.

Ellen 1:10

Before we get started with today's topic June, could you tell us, because we have a lot of trainees, could you tell us a little bit about your professional journey as far as how did you get interested in this sort of subset area within interventional cardiology, how did you get your training, and what was your inspiration?

Jun 1:29

That's a great starting question actually, Ellen. So I I grew up in Michigan. I was in medical school at University of Michigan, and I was really honestly inspired first by vascular surgery to really embrace the vascular world. At some point I actually thought I wanted to become a vascular surgeon, but at the same time, I really loved the the clinical aspect of cardiology as well. A- and I w- really wanted a specialty that would marry the two of them together and allow me to really impact the patients that are affected by peripheral artery disease. At the time that I was in medical school endovascular was really in its nascency. It's grown up a little bit now, so there's more and more of us practicing endovascular therapies out there. But really this is a pathway where one would first get training in internal medicine, then general cardiology, and then sub-specialize in interventional cardiology, and then subsequently endovascular advanced interventions. So what it really means is that we do a lot of the procedures that vascular surgery might offer, but we do it minimally invasively. So we would use guide wires, catheters devices, atherectomy devices, sometimes balloons and stents to revascularize patients that really have critical limb ischemia or chronic li- limb-threatening ischemia where they might have wounds that are not healing for months or weeks and th- these are patients at risk, very high risk of major amputation. Now, you may ask why did I get really started in the PE space. So as I was doing my training in my final year of interventional cardiology and endovascular, that's when a lot of the new devices were actually out on the market. They had just introduced the thrombectomy catheters, the large bore thrombectomy catheters at the time. And that's how I really got started in the PE space, and we were honestly all just learning at the same time. We were trying to figure out who are the best patients patient selection-wise, to undergo a thrombectomy, the procedure for pulmonary embolism. Or who are, who might be the better patients for catheter-directed thrombolysis, and who are the patients who will just do fine with medical therapy. I would say we've learned a lot in the last decade in terms of parceling out which patients would benefit. But there's a lot more that we are still undergoing research trials on to under- really understand are these patients going to be fine on the long-term status with just medical therapy alone. So it's a very exciting time to actually be in this field because there's so much research going on to really fine-tune our management on this complex disease.

Ellen 4:23

That is wonderful. And with all these exciting developments, we now have our new ACC/AHA guidelines on PE. But before we start with that, I think I just wanna go back a little bit to the basics because we know that diagnosis of PE really starts with having a high clinical suspicion. And so for our general cardiologists and our APPs, et cetera, can you just talk a little bit about what features of a patient's history or physical exam really make you suspicious for having a PE?

Jun 4:57

The the classic kind of Virchow's triad of risk factors for DVT formation is actually very important. So remember that clots form when there's static blood. So the patients that generally speaking are at slightly higher risk of having DVTs include those ha- that have been sedentary for whatever reason, so that may include long-haul travel. When we think of long-haul travel, it's really four hours or longer of flight time or driving distance time. Long-haul travel recent hospitalization the patients who are sedentary for other reasons, for example, they may be recovering from knee surgery, just as an example. The patients that are laid up for other reasons or who might be a little bit more immobile because of body habitus. Those are the kind of more traditional risk factors that we think of for somebody who might be a little bit more static. The other-- there are certainly other risk factors such as malignancy a family history of VTE, so genetically predisposed to having DVTs and PEs. Patients that are on hormone therapy can also be at risk. The patients that are exposed to certain viral illnesses and we learned that quite robustly during COVID actually is that the patients that are exposed to COVID have a higher propensity for developing thrombus. I've noticed actually a pattern that there are other viral illnesses out there that can actually predispose patients to having VTEs as well. So it's not purely just COVID, we just happened to see a huge signal during the COVID era of P- DVT and PE in patients who developed COVID. So those are some of the traditional risk factors that I would think of. When we think about DVT development what patients typically report is edema typically in one lower extremity, but certainly you can have DVT in bilateral lower extremity, so I wouldn't necessarily say that patients with bilateral lower extremity edema don't have a v- don't have findings of a DVT. But usually it's unilateral. Usually you would see erythema, pain and obviously in the very severe cases, you may feel a cord on palpation on physical exam. A lot of times when patients present with PE, they usually develop either su- very sudden onset shortness of breath or chest pain. These patients when they're really critical, meaning that if the PE burden is really high and they suddenly causes a abrupt change in the RV hemodynamics meaning that with the obstruction in the pulmonary artery, especially in large burden pulmonary embolism, the right ventricle is going to suddenly dilate, and that can decrease your preload as well as decrease LV function from the RV dilation. So those patients may actually present with presyncopal or even syncopal episode. And at the very, very critical extreme would be the patients that really are coming in with refractory cardiogenic shock or even cardiac arrest as a result of the RV dilation and the spiral

Ellen 8:22

Wow, thank you for that review. So at this point, we are gonna turn our discussion to the new ACC AJ- AHA guidelines on PE. In fact, these are the first ever USA joint society guidelines on this topic.

Kanny 8:35

Yeah, thanks, June. The new guideline document is excellent because it really seems very clinically focused I know it still endorses D-dimer as part of that initial laboratory assessment, especially after you've done a clinical assessment with some of the clinical pointers you just mentioned. Is that still the initial test for low and intermediate suspicion patients or is there still a group of patients where you might go on to more advanced imaging right after the initial history and assessment?

Jun 9:06

That's a great question. So the patients that are low clinical probability, meaning that could there be something else that have-- that would have explained the shortness of breath could it have been COPD or heart failure. In patients with low clinical probability you would apply the PE rule out criteria or PERC, P-E-R-C. You would first do the PERC rule and then based on that if all criteria are met, then you probably don't need to do any further testing. So meaning that the patient has ruled out for PE. Then if the patients don't really rule out based on PERC or those patients that have more of an intermediate probability. So say, for example, maybe they don't have all the things that I listed present, but maybe they're on hormonal therapy. And you kinda have this intermediate probability of maybe the patient has a blood clot. D-dimer is a great first test to understand whether or not the patient has the po-probability of PE. However, as we all know, D-dimer can be elevated in other situations. Inflammatory states, for example can actually falsely elevate your D-dimer. As a result, we actually do recommend the usage of the years criteria which looks at the probability of DVT. For example, in addition to D-dimer, et cetera that we can then discern whether or not the patient has a likelihood of PE or DVT. In addition to DVT on this year's criteria, we also look at hemoptysis and whether or not PE is the most likely diagnosis. As you can see, a lot of this is actually contingent on your clinic-- your own clinical suspicion now we have in the guidelines then outlined based on the years criteria and the D-dimer, should one then proceed with PECT, for example, or a VQ scan. So depending on what your D-dimer is in combination with the years criteria for this very specific intermediate group or those who met-- who didn't meet any of the PERC rules then that would be the algorithm to follow. So there are patients that have D-dimer that are elevated and/or years criteria that m- that was significant, then the formal recommendation is to perform diagnostic imaging. The patients that really you have a very high clinical suspicion where that the leg is swollen, it is red, they have significant hypoxia with shortness of breath, and those are the patients that upfront you probably should just go for a diagnostic imaging where your clinical suspicion is high enough.

Kanny 11:51

And that's very helpful. So CTPA still sounds like the definitive confirmatory test. Obviously Ellen and I, we're both echocardiographers, and most of our cardi- clinical cardiologists understand the echocardiographic criteria as well. But is it still the case where an echo's really not sensitive enough to make a diagnosis? It can just perhaps confirm it if certain criteria or certain findings are seen?

Jun 12:17

That's a great question. So echocardiogram it can be good augmentative testing. I think especially in patients that are too unstable potentially for a CT scan or VQ scan. However, the problem is, as you all know, the RV can be dilated in the setting of other disease states including chronic pulmonary hypertension as well as left-sided heart failure as well. So there, there can be other etiologies for RV failure, so it's not end all be all. In addition, it's really RV failure, we see RV dilation when the clot burden itself is high enough. So you may not necessarily pick up the patients with smaller PEs or subsegmental PEs. Certainly an important augmentative test. We've also recognized as part of the guideline writing committee that not everyone has the ability to do echocardiogram in the middle of the night. So we actually advised against a formalized requirement for every patient to receive an echo on the, at the time of diagnosis of PE. We know that our echo's gonna be very important in terms of prognostication for the RV. So we didn't make it a requirement to get an echo, but certainly that can be augmentative information.

Ellen 13:44

Wonderful. Thank you. so in fact, one part of the new guidelines, which I find really quite interesting, is this new classification of severity of PE upon presentation ranging from A to E. Can you please discuss what puts a patient into each of these categories? And also, what are the implication of these categories with respect to treatment options for each.

Jun 14:05

The new classification scheme I know it's very different than what we were traditionally used to. Back in the day, in the early 2010s the United States guidelines actually recommended the use of massive, submassive, and low risk PE. The Europeans then in the later 2010s recommended the use of high risk, which correlated with massive PE intermediate high and intermediate low risk. So they went ahead and divided the sub-massive category into two, and then they maintained a low-risk category. Just for simplicity's sake what we really ended up doing on this current iteration of guidelines is we really fine-tuned a little bit more within that intermediate high-risk category. So right now when the patient has true pul- cardiopulmonary arrest so meaning these are the patients with refractory shock on multiple pressors or have had a cardiac arrest or if they're on supportive mechanical c- circulatory support like ECMO, for example, these patients are truly in the cardiopulmonary failure category, which is category E. These patients truly correlate with what we used to call high risk or massive PE then we really wanted to fine-tune exactly which are the patients who are at risk of teetering into category E. So we took that high intermediate risk category that the Europeans had and really subdivided it into C and D, with D being the worst of the two. So D are the really the patients that have potentially a transient hypotensive episode, meaning the pre-syncopal episode or normal tense of shock. So if you have the advantage of having a right heart cath data on these patients a lot of them will actually have a cardiac index of one point six to one point nine. So these patients might appear normal tensive, but because the RV is in such fulminant failure, they are actually in normal tensive shock. And these are the patients that we do have to be aware of potentially teetering into category Es which is again, the full ca- cardiopulmonary failure. So category D are the patients that you really have to be vigilant about watching them and potentially thinking about doing a procedure or more advanced therapies earlier rather than later. So then category C are the patients that would have met criteria to be included into what was the intermediate high risk. These are the patients with abnormal RV on CT scan as well, and/or echocardiogram, as well as abnormal biomarkers. We divided the category C into an three different categories so that we can really parcel out exactly which patient cohort we're talking about. The patients that have abnormal RV findings either on CAT scan or on echocardiogram With at least one or more abnormal biomarker are considered in the C3 category. Those that have either RV dysfunction by imaging and/or or one or more biomarker that is positive, so meaning troponin or BNP elevation, those are considered C2 category. So we really parceled out within the intermediate and a high-risk category who is really sick and who is probably not as sick. And then if you think about the intermediate low-risk category from the European guidelines, that I would categorize nowadays as more kind of category B patients. And then the subclinical findings are the patients that are really truly low risk and potentially can be treated more as an outpatient. The, In addition, we introduced the respiratory modifier as well, so meaning that patients that have a elevated oxygen requirement or requiring any supplemental oxygen, depending on which category you're in. So adding the R modifier meant that the patient was potentially even sicker than what our initial category is. So it's a lot of adjustment to really change the language and how we triage these patients. And we hope that with the new categorization of patients that this will allow us to do better research to really sort out the D category patients, the C category patients who would benefit from more advanced therapies early on.

Kanny 18:57

Thanks, June. So I guess just to clarify then obviously category C or higher, you're gonna certainly hospitalize a patient and watch closely for decompensation. But it sounds like all-- just having an abnormal echo by itself that shows some RV dysfunction alone doesn't really place you into group D or E necessarily as a finding in itself. Although certainly it would still indicate a higher risk situation in group C.

Jun 19:24

That's right. So it-- the presence of an abnormal echocardiographic finding with RV dilation plus biomarker would actually even place you into C3 category. Oftentimes, when we talk about these patients on our PE response teams or PERTs we actually are specifically trying to figure out the C3 category and how many of these C3 patients really belong to D1 or D2 where they're in normal tense of shock. And that's really the art of all this, is trying to figure out which patients are belonging in which category and which patients really deserve a earlier rather than later triage of potentially more advanced therapies

Kanny 20:12

And obviously we definitely are looking forward to talking about some of the advanced techniques and the response team. But before we do that, we just wanted to ask you about anticoagulation. Obviously it sounds like this classification system in a sense guides the intensity of monitoring. Does it also affect any decisions about anticoagulation? And do the new guidelines update kind of any of the, our traditional approach to anticoagulating these patients in any way in terms of either duration or intensity based on this classification?

Jun 20:48

One of the interesting things that we debated a lot about actually in the anticoagulation arm is really whether or not to make a recommendation formally for low molecular weight heparin or Lovenox over unfractionated heparin or more traditional IV doses of heparin. The, one of the one of the issues that we've noticed kinda throughout the years of practice is that unfractionated heparin can produce a lot of fluctuations and unknowns in terms of when are we in the therapeutic range. It's taking hours to re- obtain therapeutic range, for example. So we actually formally recommended u- the use of Lovenox over unfractionated heparin as the preferred agent for patients with pulmonary embolism when they come in. In terms of therapy duration really depends a lot on the presence or absence of DVT. By and large, most patients with pulmonary embolism the thrombus even if left alone to anticoagulation without any advanced therapies generally speaking would be resolved at about anywhere between four to eight weeks. So by and large for most PEs if one were to repeat echocardiograms, say, at two or three months for the most part, most right ventricles will actually resolve to becoming more normalized. However, DVTs generally take longer for resolution. So depending on the proximity of the DVT, meaning are you looking at DVT in the iliac vein, are you looking at DVT in the femoral or popliteal vein or just tibial vein the residual DVT will potentially dictate the duration of therapy. More proximal clots, generally speaking, take longer and the more distal clots, like tibial veins, for example will usually resolve in about three months. Sometimes the therapy duration actually depends more so on the residual DVT burden as opposed to the PE itself. In my practice, the routine monitoring for patients is usually an echocardiogram during follow-up. And again, the follow-up depends. If it's a large burden PE that we performed a thrombectomy on, I may follow those patients up within a month just to evaluate to make sure they tolerated the procedure all that the shortness of breath is resolving, and the echocardiogram has normalized. If a patient has undergone anticoagulation alone, sometimes I might extend that follow-up out to maybe two or three months just to ensure that I've allowed enough time for RV recovery before I repeat the echocardiogram. And then depending on where the segment of DVT residual DVT there is, I may be obtaining a DVT scan either at six months or at nine months. So if it's really proximal, I would, generally speaking, extend that follow-up duration to nine months so that I have a better idea of the resolution of the thrombus.

Ellen 24:10

So one follow-up question for anticoagulation is how many of these patients and/or which patients would you consider needing a hypercoagulable or a thrombophiliac workup?

Jun 24:21

That's a great question. I would say, in general, not everyone needs to number one. But the... you're right. The, those that actually don't have any classic risk factors may be considered, especially if they're young. The patients that have a very strong family history of VTEs should also be considered for further workup for a hypercoagulable state. If there's a really high suspicion of antiphospholipid syndrome you really should undergo the testing even in-house before you discharge the patient. Most of us actually use DOAC and that's actually recommended as well over Coumadin because of the ease of use with DOACs. But if you're discharging a patient on DOAC a- and there's a high su- very high suspicion of antiphospholipid you should undergo testing first in the hospital to exclude that.

Ellen 25:19

Jun, that was a great discussion on anticoagulation. But as we turn to more advanced techniques, more invasive therapies that are used for these PE patients, how do we decide regarding, let's say, a surgical intervention versus a catheter-based technique whether it's systemic thromolytics versus catheter-based? Do these decisions depend, first of all, on your institution, or is it based on an individual patient characteristic such as age or comorbidities?

Jun 25:51

This is a very complicated actually question. So number one is yes it does really depend on local expertise. The regional expertise of the hospital that you're at will actually dictate some of what is offered. So from a surgical perspective, I would say the majority of institutions now probably would not offer surgical as the first line. The most- the majority of institutions nowadays should have catheter based therapies available to be offered for our patients for a little bit more minimally invasive technique. It- interestingly, when we wrote the guidelines we really only had one randomized clinical trial that was available to really help us parcel out what should we do for these patients. And that trial at the time was peerless And that was a trial that randomized a large bore thrombectomy versus any catheter-directed thrombolysis. So meaning using a very small catheter administering TPA through the catheters versus a suction device, basically. The the outcomes really on that trial was not mortality so there was no true mortality benefit for one versus the other. And the primary outcome in favor of thrombectomy was actually driven by two things. Number one was decompensation and essentially crossover of the patient to the other arm. And then the second thing that really affected the outcome was length of stay. So length of stay in ICU as well as length of stay in the total hospitalization. Whether or not if we were to look at harder outcomes for these patients whether or not one therapy is really going to be more beneficial than the other, we still don't know in this day and age. So after the guidelines were written in the last few months there are two additional trials that have come out which looked at anticoagulation versus different types of therapy in these patients that would have fallen mostly within category C3 and then some in D1 and D2. And that really depended a little bit on trial design. So the first trial that came out was the STORM-PE, which utilized a computer-assisted vacuum thrombectomy device versus anticoagulation alone. And that, again, did not show mortality outcome, but it did show RV to LV improvement. And then interestingly, a quality of life improvement at ninety days in favor of thrombectomy over anticoagulation alone so again, a little bit of a softer outcome, not necessarily a hard endpoint, but a very meaningful one, especially if you're the patient that has a PE. And then HYPITHO really came out earlier this year in 2026 which looked at ultrasound-assisted throm- thrombolysis through a catheter versus heparin anticoagulant alone. And I would say the criteria for escalation of therapy, meaning switching arms from heparin anticoagulation into the thrombolysis arm was very stringent. They used a criteria called NEWS which was widely utilized in Europe. These, this new score actually detected patients who were decompensating and they had to meet a certain new score in order to cross over into the catheter-based thrombolysis arm. So in HYPITHO again, mortality was exactly the same between the two arms. So what- whatever we're doing right now for this category C III and D patients may not necessarily impact mortality, but it certainly did actually have a major impact in terms of the rates of decompensation in this HYPITHO's cohort of patients. That being said more and more data is being generated. There are actually still ongoing clinical trials, randomized clinical trials right now that look at different types of thrombectomy against heparin anticoagulation alone. A lot of us believe that w- we're very unlikely to detect a mortality outcome in this specific patient cohort because remember, we're not studying the category E patients right now. This is category C III and some in the D category of patients. So intrinsically, their mortality rate is going to be lower. So we don't believe we will detect a mortality difference, but we believe that it likely would continue to show a quality of life improvement and potentially improvement in terms of decompensation during the hospitalization

Ellen 30:53

Actually, I have a follow-up question for you. So as you're talking about, you did mention you get interventions based on the expertise at your particular center, and obviously many centers don't have these expertise. Are there certain centers of excellence where patients should be transferred if more advanced therapies are needed,

Jun 31:14

There are actually centers of excellence supported by the PERT consortium that offer PE therapy. At a local level smaller hospitals may offer PE therapy. As a example in university hospitals in my institution we do have a true spoke and hubs model, and I think we'll talk a little bit about it in the next segment as well. But our central hospital that we perform a good proportion of PEs at is either Cleveland Medical Center, Parma Hospital or Ahuja Medical Center. So when we receive a pulmonary embolism call from a outlying hospital, say for example in Geneva, which is very far east in Northeast Ohio we may ask that the patient be brought to one of the more central hospital within our system that has the capability of performing pulmonary embolism procedures if needed. Now, I don't know for sure that at the time of the phone call that the patient will eventually need this, right? They may be falling within category C3. However, they can always decompensate. The highest rate of decompensation is usually within the first couple of days of the patient observation in the hospital. So the patient decompensates, or if on the next day we see the patient and they're just huffing and puffing and can't even say five words without taking a deep breath, those are the patients that we think would probably benefit more from earlier intervention versus not. Now again, like I said, we don't know for sure that this will improve overall quality of life long term for everyone using these types of therapies So we're extrapolating a little bit that these types of patients would benefit. But if we foresee potentially a patient requiring more advanced therapies, we certainly would have these types of patients transfer into a hospital that is capable of providing pulmonary embolism care.

Kanny 33:21

Yeah. Thanks, June. So I think that's a very good lead into a discussion about the response team. I know this has been something that's been o- over the last decade or so be- becoming developed at many tertiary hospitals. But we are curious about how you approach that at University Hospital in terms of w- what is the advantage of having a response team in place versus simply having a collection of specialists, first of all? And then secondly how did your institution approach putting that together?

Jun 33:52

So The idea behind the PERT really was started about 15 years ago by Kenny Rosenfield in MGH. And really the thoughts, the processes in patients that are really truly critical and we need a rapid discussion on the patient with multiple experts. If you talk to 10 different PERT teams, you're going to get 10 different responses on how this is actually run. And even within our own PERT we've actually undergone some evolution a- and some change on how we've tailored our therapy to our current practice. So the more traditional, I would say, PERT really is a team that is consistent of multiple subspecialists. In our institution it's interventional cardiology, but in a different institution that may be interventional radiology or vascular surgery, or even CT surgery. So there has to be a interventionalist as part of this team, so anyone who is... has expertise in performing these procedures. we also have vascular medicine traditionally as part of our PERT and then pulmonary critical care. I would say we've fine-tuned our team a little bit in the last few years. So we really tailored the vascular medicine involvement only really for patients that we have questions on anticoagulation, for example or whether or not safety of TPA the, at the time of the PERT discussion. So we really are fine-tuning i- in terms of when to involve specific team members. Smaller extensions of the PERT are actually CT surgeons in our institution. In patients who have, for example, cardiogenic shock from RV failure that require urgent VA ECMO we usually involve the CT surgeons in our discussion to ensure that they're appropriate candidates for more mechanical circulatory support. So the PERT team is going to vary based on where you practice and what, how it's set up in your institution. So regardless of what we decide, if the patient is transferring to a hospital where PE pro- procedures are performed, I am a huge advocate for really seeing the patient live. If it's not that night by a fellow, then it's def- definitely the next day by one of our team members to really assess how is the patient doing. There's no replacing a physical exam and there's no replacing talking to a patient on how they're feeling when they're walking around the unit, for example. So I, I think yes, the PERT team's critical for the initial triage, but really it's a very individualized decision on how to manage each one of these patients

Ellen 36:47

Wow, Junaid, it's an incredible discussion so far on the acute tr- treatment of PEs. Just to wrap things up, one question is how often do these patients who have an acute PE run into issues with chronic thromboembolic pulmonary disease following their initial PE, and is there any role for surgical thrombectomy in these patients

Jun 37:09

Unfortunately, a lot of these patients, about maybe a third of them, will still have ongoing dyspnea or limitations on follow-up. The presence of C- CTEPH or CTED that is chronal- chronic thromboembolic disease either with or without pulmonary hypertension can vary. The literature is actually very wide when you look at the incidence of this because it's un- unfortunately very often undetected out there. So for patients with CTEPH so with pulmonary hypertension, potentially the the incidence post PE is about 2 to 4% we believe. But there is a proportion of patients with CTED where they might have chronic thromboembolic disease but without the component of pulmonary hypertension, and they still have dyspnea on exertion after the PE. So it's critical for patients to undergo further testing in these situations. That may involve echocardiogram with VQ scan or even C-PET testing to really understand what are the limitations of the patient. Is this from the PE? And the, in patients that are testing positive for concerns for chronic thromboembolic disease there's a couple options out there. For patients with large burden of residual chronic clot, meaning more central performing a surgical thromboembolectomy is really the gold standard in these patients. The patients that have more peripheral disease, so meaning in these subs- it's truly in the subsegments of the pulmonary artery these patients can undergo a balloon pulmonary angioplasty, and that's actually a field that is up and coming as well. As we learn more and more about these CTED and CTEPH patients I suspect more and more centers will actually be offering these services as well to really help patients feel better.

Ellen 39:10

Well, June, thank you for an incredible discussion on the new PE guidelines with therapeutic implications. We are so thrilled you were able to join us at the Cardio Ohio Podcasts. And until future podcasts, thank you very much. Have a good evening.

39:29

Thank you for joining today's podcast. For more information about the speakers or the topics, please go to Ohio acc.org,