Hello, I'm Stanislav Hankin, the Director of the Vascular Medicine Program at Dartmouth-Hitchcock Medical Center, 11 in New Hampshire. Today I'm delighted to be joined by two intercoagulation experts, Dr. Craig Beavers, who is a Cardiovascular Clinical Pharmacist at University of Kentucky College of Pharmacy, and Dr. Theresa Carman, who is the Director of Vascular Medicine at University Hospital Medical Center. And today we're going to have a nice panel discussion on nuances of direct oral intercoagulants as part of the practical management of venous thromboembolism, simplifying intercoagulation strategies. Dr. Beavers, Dr. Carman, pleasure to be here with you. Thank you for having us. Thank you for having me, yeah. These are our disclosures, and we're going to talk about a couple of cases. Let's start off with case number one. So this is a 63-year-old woman who presents with one week of worsening right calf swelling. Her review of systems is otherwise negative. Her past medical history is significant for coronary artery disease, status post percutaneous coronary intervention to right coronary artery about three weeks prior to presentation. She had an endostomy at that time. Additional past medical history is significant for hypertension, hyperlipidemia, type 2 diabetes mellitus, and then stanchional disease on intermittent hemodialysis. These are her medications listed here include aspirin, amlodipine, atorvastatin, clopidogrel, isosorbide mononitrate, and metoprolol. Her vital signs are significant for a weight of 135 kilos. Her heart rate is 86. Her blood pressure is normal at 135 or 75. Her respiratory rate is normal at 18, with normal pulse ox and 99% of room air. On physical examination, she has one plus spinadema of the right calf, and otherwise normal exam with normal longevity pulses. Her labs are significant for hemoglobin of 14.2, platelets of 250,000, and creatinine of 6. A DVT duplex is obtained, and this is the finding that shows right peroneal vein acute venous thrombosis. So we have a couple of questions to discuss here. Let's start off with Dr. Carman. So first, a more difficult question than we actually think here, does this patient require hospitalization? So I would say at first blush, no. I don't see anything in her vital signs that would suggest to me she might have a concomitant pulmonary embolism above and beyond the symptomatic, you know, caffeine thrombosis. So I would question her very carefully about any respiratory symptoms or any chest pain, any lightheadedness, any dizziness, anything else that would lead me to believe that maybe we're not dealing with just a caffeine DVT. Got it. And let me ask you this question. If the review system is otherwise negative, and really there is no shortness of breath, there is no chest pain, would you ever consider getting a CT of the chest to rule out pulmonary embolism in this case? I tend to reserve looking for pulmonary embolism when patients have some symptoms. Now they don't have to be terribly symptomatic for me to look, but I do think they have to have symptoms. We know that with any DVT, the risk of a pulmonary embolism is about 40 to 50%, even with caffeine DVT. But if she's asymptomatic, I don't know that I would necessarily upfront decide to look in this situation. It may depend on how you decide to treat her going forward. But upfront, I would really reserve my imaging for only if she were symptomatic. Got it. And that totally makes sense. When would you hospitalize a patient who has an acute DVT? What kind of things do you think about that the patient would require hospitalization without a pulmonary embolism? So I think if they're severely symptomatic, where you may consider doing other therapy for them, such as if you're going to consider maybe an intervention, or if they're symptomatic enough that you don't feel comfortable sending them home on just an oral anticoagulant therapy. I think if they have difficulty understanding instructions, or if they're going to have a difficult time following up, and you need to make sure that they're being adequately treated. If they don't have medical literacy that's going to allow you to send them home and be their own health care provider for the first few days while you're managing a deep vein thrombosis. I think those things weigh very heavily, in my opinion. I do think a lot of patients can be treated fully in the outpatient setting. It does require a reliable, responsible patient. Can I ask a question? Because this may borderline on the next piece, but does this weigh your hospitalization consideration? Because she has end-stage renal disease on hemodialysis. So are you okay in this juncture using the direct acting agent and sending them home? Or would you consider unfractionated heparin at that juncture, admit them, kind of distills upon that consideration? Dr. Peters, that's an excellent question. I think let's start off with what are our anticoagulation options in this case? What do you think? Clearly from a, you know, when you think about end-stage renal disease, you know, obviously you have your agents that are not entirely or solely dependent on renal clearance, such as, as I alluded to, unfractionated heparin intravenously. There's obviously a lot of up-and-coming data and mixed opinions about using your direct acting agents, specifically, you know, pixavan, and we can talk more about that, or rivaroxaban, in these instances. But just, you know, considering, you know, the classic, you know, unfractionated heparin route with warfarin to bridge, you know, those are really, when you think about end-stage renal disease, those are, you know, with the dialysis picture, a lot of what you're thinking about or considering, those are really your two divergent points, the common classical thought process. And let me ask you a follow-up question. Can we use lobinox at all in patients with end-stage renal disease? Good with a lot of monitoring, you know, but that becomes not, and I'm not saying that unfractionated heparin doesn't require monitoring, but you, it would not be preferred. I mean, you can do it, and I've seen data that suggests it, but then you have to contextualize that with a factor Xa level and some of the consistencies and the kinetics associated with both the when to draw the level and understanding those items. So it's not, that is probably not impossible. It's probably not as, people are not going to feel as comfortable or easy to use that compared to, you know, classically using an unfractionated heparin drug or just avoiding using an unfractionated heparin altogether and considering the direct acting oral anticoagulant route. Your side, Dr. Korman. So I tend to not use low molecular weight heparin in end-stage renal disease. It's actually, it's a hospital policy for us for the most part, but again, I think that's, you know, in a big hospital system where you have to have hospital-wide policies to protect the majority of patients, it's a policy. And it doesn't mean we don't make exceptions, but we just would tend to not use low molecular weight heparin. And I agree with you a hundred percent. I've seen people that have done it or literature, but it is not my preference in any way, shape or form. I want to be very clear about that. I think I would come back to the question of, do we need to anticoagulate her first? Because I think if you need to anticoagulate her, it gets much more complicated. I am also not entirely a fan of even a PIXABAN in end-stage renal disease. And I find that a lot of people I don't think are necessarily as comfortable with it, even though it does carry, you know, an approval in this setting and you don't need to dose adjust, et cetera. What I tend to see is people do dose adjust, and then that also gives me a little bit of concern. So I think that it really comes back to, if you're in my clinical practice, if this were a proximal DVT, my options for anticoagulating her would be unfractionated heparin followed by a vitamin K antagonist. That's practically what we would choose in our setting. That doesn't mean they're not alternatives, but I think you have to be very careful. Dr. Carmen, I think you raised a good question, and I'd like to go back to our second point here. And the question is, would you even anticoagulate this patient, meaning would you treat this patient? And I'm asking because our chest guidelines do suggest that with caffeine DVT, you may have a choice whether you want to treat these patients with the anticoagulation or you may decide to follow them with serial duplex for proximal DVT. In somebody like this, with a patient who seems to be somewhat symptomatic with some edema and maybe discomfort, what are your thoughts in treating this patient? I'm going to be honest. I would probably follow her with serial duplex. I would put her in compression to help with the inflammation, and I would probably follow her with serial duplex and encourage her to ambulate. It depends partly on how easy it is for her to get back for serial ultrasound. But the fact that she's on dialysis, she probably has healthcare access several times a week, so it may not be terribly difficult for her to get back. I think in the setting of the recent PCI and the need for DAPT, adding another anticoagulant in that setting really makes me very nervous. And so I would, given that she doesn't have any symptoms of pulmonary embolism, now obviously if she has proximal propagation on serial duplex or if she has any symptoms of pulmonary embolism, we would have to go back and reassess all of those, all of those, you know, the choices that we've discussed. But I would probably put her in a stocking, try to get her past the inflammation. As long as she's ambulatory, she doesn't have an overt number of high-risk criteria according to the chest guidelines that would put her at risk for propagation. Certainly anybody can propagate, but that would, I would tend to lean to that side. That absolutely makes sense. I would agree with you too, because even the point you've raised, and on the flip side, she would have lots of risk for bleeding, right? Absolutely. And so that weighs very heavily that, and we all know, even when you get down to it in a situation like this, you know, especially for VTE and looking at even warfarin for that matter, the data is, and CKD is at best moderate to questionable, you know what I mean? And so when you really contextualize their bleeding risk in this situation, it makes you pause. So if I was on rounds with you, I would be, you and I would be echoing or singing to the same choir for that thought process. I do think too, she has to be reliable and she has to understand the signs and symptoms of pulmonary embolism. She has to be reliable with respect to following up for her duplex ultrasounds, following through with a management plan, and then be reliable so that if she develops any symptoms, you know, she'll get additional medical attention. Absolutely makes sense. So let's say, let's, let's, let's put a scenario that you, with shared decision-making with the patient, decide to undergo serial duplexes. She comes in about a week later and she has propagations into the popliteal vein. So now you're kind of stuck. You have to anticoagulate. Choose an anticoagulant and why. We talked a little bit about it, but make, what's your choice of anticoagulant to send her home on at this point? She's in an outpatient setting. What are you going to do? I would lean towards the, the admitting her and putting her on unfractionated heparin and vitamin K antagonist. You know, again, she's, she's in the institution enough, frequently enough to be able to get INR management. You could really make a case for treating her for six weeks over a full three months therapy. I don't know. That would be my preference, but you could make a case for that. I still, I still don't know that I would be terribly comfortable ideally putting her on a PIXABAN. Absolutely. Dr. Beaver, something that I think confuses a lot of us is dosing of a PIXABAN with acute venous thromboembolism compared to the dosing for non-valvular atrial fibrillation. And we know that there are three criteria for dose reduction in atrial fibrillation. Is this the same for venous thromboembolism or is the dosing different? Do we dose reduce in venous thromboembolism? Actually, if you look at the package insert for VT, there is no, especially when you get to the renal considerations, there is no alternative dosing regimen or recommendation that occurs for that. So it is distinctively different in that construct. That being said, again, as we're alluding to, people are aware of this for, it doesn't say for or against doing it, but people have tried to extrapolate and use that in this context. And like I said, there's retrospective data that people have attempted or looked at or evaluated, both compared to nothing or to warfarin, but again, I think we're not at the phase or at least I'm at the phase where I'm 100% every time comfortable reaching or recommending that even, and like Dr. Carmen alluded to, I think people do do those types of things where they get a little nervous and they dose reduce, and it may not be the right time to dose, or for example, you still have to do the introduction phase and they skip that piece of that treatment, right? And so they're doing all these manipulations to make themselves feel better and is it the right thing to do? And it may not be, or, you know, we just don't have the clear guidance on that. So in a conservative fell safe manner, like Dr. Carmen alluded, and we were talking about earlier, I think you have some comfortability and assurance with the heparin to warfarin route. And in this case, you exactly look at everything that can be in, you know, she's a dialysis patient and follow up, and I always consider the four Ps, right, of things when I think about this. You know, how did the patient present? We were kind of alluding to that. What are the patient characteristics that exist in this patient, both from a thrombosis, bleeding, or other scenario side, you know, what are the pharmacodynamics, pharmacokinetics that we have to think about, not just, you know, their CKD or drug interactions, or, you know, theoretically, if she has resource issues that we have to consider or think about, and then what are their patient adherence, like what are we going to do to adhere? So I think about all these things when I'm considering the overall situation and weighing the pros and cons of what should be going on. So yeah, and one additional thing I would just like to note is that she was 135 kilos as well. So my question to both of you, even, you know, if there is no real insufficiency, does that weigh at all on your choice of an anticoagulant? Can we use direct oral anticoagulants in sort of the extremes of weight at this point? What's the evidence point to? Dr. Carmen, you can go first, and then Hannah. So I would say with the most recent ISTH guideline update suggests that at this weight, we could use a DOAC if we so chose, with the strongest data being for rivaroxaban and some data also existing for pixaban from the clinical data that's available. I would say I also do look at BMI. You know, historically, if you went back to the first guidelines, it was for BMI greater than 40 that we sort of had that cutoff. They also took away the BMI guideline. However, I will say that, you know, in the Midwest, we deal with a fair number of obese patients. And I don't know that I look at somebody with a BMI of 40 or 41 or 43, the same way that I look at patients that come to my clinic who have a BMI of 55. And I don't know that I still have absolute confidence in the DOAC across all BMI ranges that likely, like, you know, as has been, you know, projected. So, you know, DOACs now have data and have recommendations from pediatrics all the way up to the super morbidly obese patients. And while they do have a very broad therapeutic window and the pharmacokinetics, pharmacodynamics are clearly different for, you know, pediatrics and for our young patients compared to our elderly patients. I think at 135, as long as her BMI was okay, I'd feel okay. But you know, if she was exceptionally short and her BMI was 50, I'm not sure that I would feel okay. Very long answer. You and I are in the same camp on that. I was going to say the exact same nature of what you're alluding to, both, you know, pointing to people to be aware of the updated ISHT guidelines or recommendations, if you will, in exactly that piece. I think if I think about it in my practice, I feel more comfortable, yes, if it was 135 and we knew, you know, she was a taller individual or, you know, something that's going to affect her BMI to the extent that, you know, she's in that threshold, I definitely feel super comfortable in that, you know, the 30, 40 range from that perspective. If you get to these super extremes of either side of the weight paradigm, I get a little bit nervous, you know, with that being said, you know, here's where you're always going to have, and Dr. Carmen alluded to exceptions, there's always going to be clinical scenarios where you may not have a choice, right? It's going to be the patient's never going to come back for X, Y, and Z or whatever that may be. And so you may have to take that chance and risk. But I think, you know, again, the key to this is in any of the situations is assuring that the patient knows that they need to continue to follow along and be in tune with any symptoms or changes when this happens, right? And understanding if they had a therapeutic failure, was it truly a failure, right? Did they, were they adhering or was it something else? You know, and I think being able to address those points. Excellent points. And I'd like to just finish off this case and say, Dr. Carmen, if this patient were to be hospitalized a year down the line with pneumonia, she was in the hospital for three to four days, are you worried about future post-hospital DVT PE risk at all? What would you do for a patient like this? Yeah. So I always make the point to my patients that if you've had a DVT, you need to make your healthcare providers aware because let's face it, we can do a hundred heart caths and maybe one ends up with a DVT, right? This is, so she already suggests to me that she may have something underlying that, that we need to pay more attention to. So for future prophylaxis for her, given the end stage renal disease, I think she is only an unfractionated heparin candidate. We don't use low molecular weight heparin again in our institution with end stage renal disease, but I think she should have pharmacomechanical prophylaxis. And so she would need SCDs on or intermittent pneumatic compression during her hospital stay. We would encourage her to be out of bed, make sure she's ambulating, you know, doing all those things to prevent a secondary event. You know, we know one of the biggest risks for a DVT is the fact that you've already had one in the past. And so we certainly want to prevent any additional hospital acquired events in these patients. Excellent. And just real quick, before we move on to this case, I know we have a bullet in there about, you know, what about her antiplatelet regimen or considerations with the recent PCI? You know, I definitely think the three weeks and ultimately if she followed back up the four week mark, I would probably for sure consider removing the aspirin or coming up with the strategies that would reduce our risk of bleeding in that particular entity. And, you know, we have the ACC has great expert consensus guidelines and these types of scenarios to consider. Of course, you always have to evaluate the risk benefit and where the stent was and those types of things. It's never as easy as, you know, this is the answer, but I think putting all the pieces together and trying to really optimize everything. And I think that's, to me, always the essential message with any of these types of patients. They're all unique and are not as easy as it's just like, this is the answer because you have a lot of things to consider. Excellent. Excellent discussion points. Can I add to one? Can I add one thing? Please. Sorry, Stan. Can I add one thing to that? I will say that as a vascular medicine person and managing venous thromboembolism, one of the things that I always suggest to people when there's a need for dual antiplatelet therapy, or if a patient is already on dual antiplatelet therapy, I involve the cardiologist that did the PCI who knows the anatomy, who knows what type of hardware might've been left behind. Similarly, if patients are on dual antiplatelet therapy following a vascular surgery, I want to make sure that the person who's managing the need for that or the proposed need are involved. It should not be a unilateral decision, in my opinion, for me to stop that in favor of my therapy per se, if that makes sense. No, absolutely. I think understanding there's a lot that goes into even where the stent and the location and what they may know that is helpful to put in context, for sure. Absolutely. I think the balance between thrombosis and bleeding is key. We, I think, can talk about the bleeding from the anticoagulation standpoint and thrombosis risk from the VTE standpoint, but talking about interventionalists, whether it's a vascular surgeon, interventional cardiologists who understand the utility and the significance of the arterial thrombosis, stent thrombosis is also key as well. Thank you for that discussion. I'd like to move on to our next case. This is a 27-year-old woman who presents with one week of pleuritic chest pain in Disney and with climbing two flights of stairs. Her past medical history is significant for seizure disorder and her medications include carbamazepine and she's on combined estrogen, progesterone contraception. Her weight is 95 kilos. Her heart rate is 95. Her blood pressure is 120 over 75 with normal saturation and room air. Her physical exam is normal. These are her labs, which are essentially unremarkable except for an elevated D-dimer for which then imaging is obtained that she was bilateral segmental pulmonary embolism without right ventricular strain. So these are some questions that I would like to discuss. Again, does this patient require hospitalization, Dr. Karman? I think in the current ASH guidelines, as well as the current American College of Chest Physician guidelines, given that she has a low risk pulmonary embolism without RV strain, without biomarker positivity, she's doesn't have any interstitial tachycardic, she could potentially be managed as an outpatient. I would probably feel better with her in the CDU, at least for 24 hours. I have not historically managed a lot of these patients in the outpatient setting, but she would, frankly, qualify for outpatient therapy if we were inclined to do so based on just those clinical criteria. However, I think she has other things in her history that might make me a little nervous about that. And let me ask you, if you were thinking about outpatient follow-up prior to discharge from the emergency department, do you ever think about additional imaging such as an echocardiogram? Do you think about low extremity duplex? Anything else? Is that routine for your pulmonary embolism patient? What's your practice? That is routine, both of those are routine for us in our clinical protocol. So our emergency department protocol considers all of the things you've already presented, but it also includes a duplex as well as a bedside echo. Now I prefer that that's not an emergency department echo, I prefer that that is our cardiology fellow going down and doing a cardiology echo. But yes, both of those would be included. And Dr. Beavers, what are our anticoagulation options in this patient now? So up front, and if the keen eye paid attention to the fact that she has a seizure disorder and is on carbamazepine, that creates a lot of challenges, especially for the consideration of our DOACs, because carbamazepine is an inducer and so induces those CYP3A4 enzymes, which become problematic for those particular agents. So unfortunately, you know, in the short term situation, I would probably use a low micro rate heparin and a warfarin to determine, you know, to get her on therapy and manage at this particular juncture. Now if we have a bullet down there that changes in medications long term, you know, as you work with, you can take a holistic approach and maybe work with the neurology team or the group to figure out if there's a reason that this is the agent of choice, or if we could switch her to something else if she's going to need it long term, because, you know, over time, you can change that, you know, induction or regulation of those enzymatic activity and consider her for a DOAC, but just given the carbamazepine at choice, you know, it'd be hard to appreciate what the effect of that's going to be unless you're able to monitor or assess, you know, her direct acting oral and coagulant levels. What are your thoughts, Dr. Carmen? No, I agree. I would not, I would not use a DOAC in this setting because of the, because of carbamazepine. We would, we would use low micro weight heparin to warfarin or low micro weight heparin monotherapy, I suppose is also an option if she chose that, but, but it would, it would not be a DOAC. And we, you know, we, we think of direct oral antagonists, anticoagulants usually as having, you know, significantly less interactions than vitamin K antagonists, but there are some specific scenarios where, where they may not be the case. Dr. Beavers, can you talk about for a few minutes about those interactions that you really worry about using direct oral anticoagulants? You know, literally when I think a lot about it, I think specifically for the, most of the DOACs, the CYP3A4 kind of interactions that we already alluded, and I do want to, to be cognizant to tell you that this interaction would also occur with warfarin, but the, the opportunity there is you have the ability to assess and monitor where they are in their therapeutic spectrum. You know, there are some kind of interactions with, for example, dabigatran, depending on where they are in the renal function with P-glycoprotein, P-glycoprotein inhibitors. So if you're talking about, you know, dronetarone, for example, and you're on the lower end of the renal spectrum, you may need to do some dosing adjustments there based on the inhibition that can occur from that perspective. And, and so really kind of paid attention and being cognizant of those. I think the falsehood that you want to get in to not forget about is that there is still the opportunity for those agents, you know, I always think, or I put it in cans and buckets of things that are easy to recall, like, you know, for some reason they're using, they have HIV and they're using protease inhibitors. You always want to be a red flag right there when you're thinking about this. When you're thinking about antiepileptics, you always want to pause when you see them. It's not that all antiepileptics are a problem, but those should be the classes of medications that if you can't recall them, you should be like, okay, I need to check and see if there's going to be a problem with these particular agents. And so that way, if you're not in tune or remembering every specific agent, you can say, these are the agents that are typically the problem, the classes of agents I probably need to be aware of. And there, there are some other ones that are off, offshoots. If you think about, you know, for some reason they're using verapamil or whatever that may be, but just really, you know, paying attention to those, those, those considerations. And, and I, and both of you quickly mentioned, at least thinking about levels, there is, you know, many of our labs now have a pixivan levels or reveroxivan levels. Thinking back to our, you know, first case into this case, would, would the levels be helpful at all? Is that something that you would consider? How would you use them? Dr. Carmen, what's your practice? Yeah, so our lab does not do levels. And I'm going to be honest, levels are not well validated. So while there have been some suggestions through like, you know, ISTH and things like that, that, that monitoring levels are, you know, are an alternative, you know, if you're going to use these drugs, you know, outside of, you know, sort of your comfort level or where it is appropriate. I, I don't measure levels. I, I have had the rare occasion where I've wanted to get a level for purposes of compliance. And at least at our facility, it's a send out and it comes back in seven days. And that's not helpful. So, so I unfortunately have to practice without levels. I have to, I have to follow guidelines and I have to make good clinical judgments, which I will be honest, patients are not always as happy with, with that. They want levels two at times, but I, it's just, for me, it's not an option. Yeah. And I think a lot of people suffer from us, including some of the same logistics that you're alluding to. And even if you didn't have access to them, you, you said it right there, we don't really have good correlations of what this is supposed to mean. And that was practically done by design, right? They didn't want us to, but there are times if you're able to get them in timely fashion, you can use them qualitatively, but not necessarily quantitatively to help you make kind of decisions from, from that particular standpoint. But I, you know, I think the good news is in, you know, 95% of situations, you don't really need them anyways. So it really, and especially as you think about the obesity question that we had coming up, I think you can feel a little bit more comfortable than when you first started out with, with DOAC saying, okay, I feel comfortable with this. It's really the extremities that you have to worry about when you come across them and so forth. But at this juncture, you can use them qualitatively. And most likely, if you have factor 10A activity or ability to assess in your local institution, you can still get a qualitative assessment without even having to use a special assay to understand, you know, you're not using to make therapeutic decisions. You're just like, okay, what kind of may be going on here or something like that? You know, if they're not taking their therapy, their factor 10A level, a normal factor 10A level, even though not calibrated for this, should, if it shows nothing, then there's something wrong, right? So I agree with you. I, we, we do have these levels available at our institution at this point, and we have both the peak and the trough, but getting the timing correct and understanding how to interpret it correctly is, is I think very difficult, because remember, we still can't, there is no adjustment for direct oral anticoagulants with these levels. So if your level is too low or too high based on your own laboratory, it's not like we should be increasing or decreasing the dose. So I've used it in the past with individuals who have had very high BMIs and were unwilling to take Warfarin, and I did it to make myself more feel better about it. Um, but, but I think now with more guidance, uh, that we may be, you'd be able to use direct oral anticoagulants in some cases of obesity. Uh, I think that the reason to use these levels is probably becoming even less and less at this point. I'd like to finish off with, um, a question for Dr. Carman. And, um, if you're seeing this patient in your, um, venous thromboembolism clinic, what's your long-term anticoagulation plan, or I guess short-term anticoagulation plan? What are you going to tell this patient about how long she should be anticoagulated for? So, um, that's a, that's a good question. I think if we go back to the case stem, um, we would be inclined to suggest that maybe this is related to her oral contraceptive. Um, I would certainly want to know if she had had any recent travel, any trauma, any injury, is there a positive family history? Are there other things that I need to know about, um, to help me make the decision? If this is, if, if we come up with no, nothing else, and we think that this is estrogen or progesterone related, I would treat her for a minimum of three months. I would change that therapy, um, and, uh, try to get her on an alternative form of contraception. Um, and, uh, and then I would talk to her again about risk of recurrence, about the need for, you know, prophylaxis, uh, potentially with she were to be pregnant and things like that. I think one of the key determinants, uh, for me is, is always figuring out why, uh, somebody had this. Not that I would, you know, start a long thrombophilia search on her. I would not do that, um, particularly in the setting of the estrogen, progesterone, and in the absence of a family history. Um, but I, but I think that you can, you can reliably say for a primary event, a minimum of three months, and then you have to have just discussions about what this means going forward. There are a couple of risk scores that have been used, um, in different scenarios for thinking about long-term anticoagulation. Is that something that you would use for a patient like this? Do you use them at all? Just a last quick minute about your thoughts about these risk scores. Sure. So I, I do use them. Um, I would use them. So for example, if we, if we talk about the dash score for her, her score would be low, right? Because she has an estrogen on board. She's a young person. She's female. And then depending on what her post-treatment D-dimer is, you know, her score would be low. So you would probably not have issues taking her off. So I do use, uh, all of the risk scores, um, and I use them not as much to help me decide to take somebody off per se, but if I'm justifying keeping them on, I want the patient to understand what their calculated potential risk of recurrence is. Does that, if that makes sense? Absolutely. So, so I will sit with them and pull up the risk score on the computer, show them how they calculate out and explain to them why I think we need to continue. Excellent. Any, any, any last thoughts? I agree. I, I think it is a, it is a great means of having a conversation from a shared decision making perspective and, and, and saying, okay, here's where we're at and risk benefit. And you know, what, what we need to do. I think in her scenario, as she alluded to, I clearly, I think looking at this, not giving that you've told us any other factors, you know, I would definitely hang my hat on this being an estrogen progesterone type situation and, you know, how to make the modifications there from that. So I, I would agree with Dr. Carmen. I would, I would ask Dr. Carmen briefly, you alluded to, you know, you didn't have a family history or no reason to do any other testing. Suppose there was something that clued you into it. And just to give our listeners another case scenario, suppose, you know, she became positive for, or it was positive for antiphospholipid syndrome. What, what is your anticoagulation strategy in those scenarios at this juncture? Yeah. So I would still, I would use low molecular weight heparin for warfarin or low molecular weight heparin monotherapy. I will say one of, I do a lot more antiphospholipid antibody testing now, particularly in patients either in her setting with a low clinical risk or in an idiopathic events because I don't want to I would like to avoid putting somebody with positive antiphospholipid antibodies on a DOAC. I think when you have alternative therapies, choosing between your therapies wisely is probably the best thing you can do for the patient instead of trying to squeeze everybody into one or two boxes. So I do a, a much more antiphospholipid antibody testing now than I probably have historically. I will say I've also had a couple of my patients who with antiphospholipid antibodies had been put on DOACs by outside physicians and came back with catastrophic events. So it's just in my mind, one of those things that's not worth the risk. Sure. I would agree with you. That's why I wanted to throw that other scenario. Sorry, Dr. Hingham to throw that in there, but it was a good time to ask. I think that's, I think that's an excellent point. You know, you really got to take every detail of a patient. You know, there is no sort of one thing fits all. We have, we have a lot of choices, choices these days with different directorial anticoagulants, but also vitamin K attack and it's a heparin. So really, you know, multidisciplinary approach is key in my opinion. That's why it's so incredibly important to have your pharmacist, your vascular medicine physicians, cardiologists, hematologists, teamwork here is what really improves patient care in my opinion. Well, I would tell you there's a lot of unique models that are being explored too about, you know, hospital at home type models. And so things that you probably might not have thought about previously, you can consider. So if you have a patient that unfractionated heparin may be better or something, you know, as care models evolve, there are even more choices because it's not even just about, here's the drug. It's okay. How can we implement X drug? So you're absolutely right. It's a team-based function. Excellent. Well, thank you for this excellent discussion. I would like to again, thank Dr. Beavers and Dr. Carmen for joining me today. And I hope that you learned a lot. And thank you to the ACC. Thank you.

venous thromboembolism

VTE management

direct oral anticoagulants

patient cases

anticoagulant therapy

end-stage renal disease

follow-up and monitoring

pleuritic chest pain