Chapters Transcript Lecture Video: Anti-coagulation Strategies (June 11, 2025) Featuring: Dr. Stephen Black; Duration: 13 Minutes; Language: English only. Right, so I'm just gonna cover anticoagulation strategies. Um, uh, we know, uh, a lot about the background of DVT and how many people are affected by it and how many people get post-thrombotic syndrome. Uh, and we also know that about 30% of the patients we treat will get some degree of instant thrombosis, uh, and anticoagulation is really a crucial part of that. There's a lot of new drugs now either called Noax or Doax uh uh that have come onto the market and I'm gonna try and cover some of uh the fact that we, we kind of really uh struggle in making decisions on this because there's no clear evidence base to decide what treatment you're gonna do and, and I think there's been a lot of variation. Uh, all around the world in this, but fortunately, we're starting to get to a slightly more consistent, uh, regimen. Uh, when you're thinking about anticoagulation, it's kind of important to think about the different levels that we, uh, treating. So the non-occlusive, non-thrombotic, Mathernococcus syndrome, Nivel patients really don't need much anticoagulation, and, uh, there's lots of variability there from just using antiplatelets to using uh short durations of uh oral anticoagulants after intervention. My personal practice is 6 weeks of a DA at at a low dose, uh, but equally some people just use antiplatelets. So those patients are gonna stay open pretty much whatever you do. Uh, you've just got to decide what you're most comfortable with in, in dealing with them. And then the the acute iFfemoral DVT in chronic venous disease patients present a slightly different challenges uh for anticoagulation strategies. Uh, acute DVT, uh, we rarely treat with, uh, the, the standard protocols, uh, regardless of whether they're having a stent or not. And chronic venous disease is, is a lot about trying to keep things open when you're compromised with inflow. So the hematological management is, is the most important. Uh, it's a prevention of thrombus propagation, trying to minimize embolization, you're trying to reduce recurrence. Uh, but the optimal anticoagulation strategies are really completely clear. There's a lot of different anticoagulants, uh, warfarin, we know, uh, reduces various clotting factors. There's some that potentiate the activity of antithrombin, which is the heparins. Uh, if you're using heparin, particularly unfractionated heparin, I've been caught out in DVT patients by treating patients with antithrombin deficiency, uh, and wondering why things don't work. So if you find patients are clotting on heparin, you would want to check for antithrombin deficiency. And now we've got some uh different drugs that are direct inhibitors of 10A, which is rivaroxaban, apixaban, and doxaban and direct inhibitors of factor 2A, which is Dabigoran, and argatroban, which can be given intravenously, and we tend to use intravenous argatroban in antithrombin 3 deficient patients uh uh who come into the hospital. Uh, and this is just a reminder of where all these things are working and some of the newer drugs, so Betrixaban and a few others that are, uh, not yet available, uh, as they're starting to try and develop them and Fondaparanax, of course, is an alternative to warfarin, we commonly use that. Uh, so just to remember how quickly drugs work. Uh, warfarin takes 4 or 5 days to get to peak effects. The advantage of course is it takes a few days to stop working. So you have patients have some, uh, forgiveness if they miss their drug. If you don't take the, uh, the Doax, they stop working very quickly. Uh, so Dabigoran. Uh, apixaban, doxaban river roan, you can see, uh, the half-life, uh, particularly for river Roxaban is very short. Um, and it takes about 2 hours for peak effect. So if patients do not take rivaroxaban consistently, then they will have problems with blocking their stent. And it's for this reason that where we've looked at our DA, we've tended to use pixaban because apixaban has a slightly longer half-life, and you take it twice a day, it means there's less chance for the patients to make a mess by not taking the drugs as we need them. Uh, and riveroxpan in particular is very heavily influenced by food, and a lot of patients don't take it at the time of their meal. Um, there's a number of trials that have been done in all these studies, rivaroxaban, apixaban, and doxy and, uh, which you can see, uh, at the bottom, the major bleeding has been similar to warfarin. It's less with rivaroxaban and apixaban compared to warfarin, and some of these trials used heparinlein, which has been important for how we've decided on stenting anticoagulation strategies because heparin nin is, is helpful, we think. Uh, cancer was slightly different. Um, the DAX now can be recommended in patients with cancer associated thrombosis. For a while, we didn't use DAX. We stuck with low molecul weight heparin, but now the, the, the, the studies have shown that DACs are as effective as low molecul weight heparin in cancer patients, which has, uh, made a difference. So one of the advantages of DAx are rapid onset, uh, uh, greater antithrombotic activity with similar or lower rates of bleeding, no monitoring. Uh, you can use them in cancer, predictable pharmacodynamics, uh, and, uh, minimal influence of co-medications and food are the main issues. Obviously in Japan, licensing of certain drugs is, is a factor for your decision making. Uh, rivaroxaban, uh, we use a lot for treating DVT and PE and preventing recurrence long term. Apixaban is our main option with the stent patients now, so we use rivaroxaban in acute DVT patients. If we're not going to intervene, we use apixaban in patients that we have done an intervention on. Uh, uh, this paper had for some time concerned us with stenting, whether there was an advantage of warfarin over DOAC. Uh, and for the early part of our practice, we tended to use warfarin for the 1st 6 months and then switched to DAC afterwards. During COVID, this changed because we couldn't bring people back for monitoring, so we started using DAs more. Frequently and when we've looked at our data now comparing those two time periods, probably there's a small advantage for the DAX, so this concern about metal and warfarin was probably unfounded. Uh, platelets in venous thrombosis is, uh, controversial. Um, uh, uh, some of you may know my colleague Adam Gudz, who did his PhD on this in our unit, looking at platelet function in venous stents, and, uh, I would say, uh, uh, when we look at some of the studies where anticoagulation and antiplatelets have been given, it seems to have an advantage. There is definitely a role for antiplatelets in venous thrombosis. It's not yet clear. Uh, but, uh, what I would say in those patients with low bleeding risk, um, and you're worried about inflow, I'm much more inclined to add an antiplatelet at the beginning to those patients in addition to anticoagulation to give them double protection, uh, which is helpful. Uh, the Saint Thomas's protocol, uh, post-venous stenting, we give low molecoid heparin twice a day for 2 weeks. And then at 2 weeks, if the duplex ultrasound is fine, we switch them to Epixaban 5 mg BD and then we consider the options, uh, at regular intervals, the 6 months to see if they need to continue anticoagulation, we may choose to stop. Uh, they all get regular surveillance with scans, 1 day, 2 weeks, 6 weeks, 3 months, 6 months, and 1 year. And if we have to reintervene on anyone, we'll add an antiplatelet. And nowadays I also add high dose statin to those patients as well, uh, because there is some evidence that statin reduces VT risk, uh, uh, in addition to the antiplatelets. Um, lots of people ask about thrombophilia and deep venous stenting. Uh, if we look at inherited and acquired thrombophilias, they are increased in the venous population, antiphospholipid syndrome being the most concerning, uh, and, uh, it was considered controversial to stent in these patients. And uh we looked at both antiphospholipid and the inherited thrombophilias, which is factor 5, Leiden uh uh mutation, prothrombin gene mutation, protein C, protein S deficiency, and antithrombin deficiency, uh, which all increase the risk of uh clots in the first place. Um, Uh, the acquired thrombophilia is really antiphospholipid syndrome, and actually it's mostly relevant in patients who are triple gene positive with anticardiolipin lupus and anti-BP2 glycoprotein, glycoprotein. Those are the patients that I worry the most about. Uh, use of rivaroxaban in high-risk patients is not recommended, uh, and that paper from Penoel Blood in 2018 suggested that they had a higher risk of clotting when compared to warfarin. And so, uh, the recommendation is not to use uh DAx in patients with antiphospholipid syndrome. So our protocol really was uh in patients with no thrombophilia, 2 weeks of low molecular heparin, vitamin K antagonist or DOA for the 1st 6 months, and then from 6 months onwards, DOA inherited thrombophilia is the same thing, low molecular heparin, vitamin K antagonist or DOAC, uh, up to 6 months and then DAC thereafter in acquired thrombophilia with antiphospholipid syndrome. They should be on vitamin K antagonists for life. Um, we looked a little bit at the difference between patients to see if there is, uh, some difference between the thrombophilia and non-thrombophilias. Uh, and we looked at consecutive patients we treated over a five-year period. We had 135 of those 130 patients, 55 had a provoked DVT, 75 were unprovoked. So roughly equal splits of the unprovoked DVTs, half of those patients had a defined thrombophilia and the other half did not. So even an unprovoked DVT we don't often pick up uh thrombophilia. Uh, of the thrombophilia, 19 or half of them were inherited and the other half was acquired, which is antiphospholipid. My hospital is a center for antiphospholipid treatments, so we do see more of these patients sometimes than other populations potentially. Uh, this is what those patients look like in terms of age and distribution. Uh, and when we looked at the results for people who required reintervention, uh, there was no real difference between re-intervention rates between provoked and unprovoked DVT. The lines were separated, suggesting that unprovoked DVT had a slightly lower rate of reintervention, but that wasn't significant. Uh, and the same in terms of patency, there was no real difference in patency between The provoked and unprovoked DVT patients uh over time and there was really no difference for thrombophilia or non-thrombophilia patients at all. So the message here is that, uh, again, patency was the same, that patients having a thrombophilia is not a reason not to treat patients. As long as you manage the anticoagulation well, they do exactly the same as patients who, who uh do not have a thrombophilia. The adequate anticoagulation is the most important. And inherited or acquired thrombophilia was not associated with patency loss or higher risk of re-intervention. Uh, so we should not be excluding those patients from venous stenting. We just need to make pay careful attention to anticoagulation. And so then your question is, do you need to uh do a thrombophilia testing criteria? So, uh, first of all, you have to check against your national criteria, should you even test for thrombophilia, and most patients do not require testing. So if they don't require testing, your options for treatment are then vitamin K antagonist or DOA uh uh for the 1st 6 months and then DOA from from then on afterwards. If they do require testing, mainly we're trying to test for antiphospholipid syndrome, which is the only one that really matters. Uh, if they do not have antiphospholipid syndrome, you can treat them in the same way, which is vitamin K antagonist and DAC. Uh, out to a year and then in one year, you make a decision on longer term anticoagulation. If they have antiphospholipid syndrome on testing, then you're gonna give them warfarin. And this is the main reason for thrombophilia testing is to decide whether somebody has antiphospholipid syndrome because the others don't really matter. Uh, so that's just the talk on, um, uh, the, um, thrombophillias and I'll just Created by
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