Thank you, Mr. Chairman. It's a pleasure to be here. It's actually a thrill, just as I came in, I met one of my old teachers who actually taught me 20 years ago how to have complications. So, anyway, we're going to talk to you today about the lessons we've learned from Bruise Control 1 and 2 about pocket hematoma prevention. So, these are the disclosures. So, the issue with pocket hematomas, of course, is balancing the risk of thromboembolism against perioperative bleeding. So the perioperative risk of device surgery can be estimated a little bit on the annual risk. So if you have a mitral valve replacement patient and a 17% annual risk of embolism, then if you stop the warfarin for 8 days, then the risk over those 8 days is 0.4%. We have better data from the DOAC trials. There's now been three papers that show that patients who have temporary interruptions of their DOAC therapy for whatever reason, then their risk of stroke very quickly goes back to what you would expect if they weren't on DOAC at all. So that is the one side of the balance that we're facing. So, this is lesson one. And lesson one is hematomas are bad for patients. And these are four pictures of hematomas. And the question is, what's different about this hematoma, this hematoma, this is actually me with a big hematoma, and this hematoma here? Well, number one, patients don't like them. They're very painful. We have a paper coming out looking at the pain that patients get after device therapy from the bruise control trials. And by far and away, the strongest predictor of postoperative pain is hematoma. Number two, they can actually lead to prolonged cessation of anticoagulation. So the very thing that you're trying to avoid can sometimes be provoked by hematoma. But far and away, the big deal about hematomas relates to infection. And this is our data from the bruise control infection study. So this was a long-term follow-up study. So the original bruise control one study patients were followed for a year after their initial index surgery. And we then looked for infection in the whole cohort. And this was the result. You know, the only predictor of infection in bruise control one was the presence of a postoperative hematoma. If you had a postoperative hematoma, your risk of infection was 11% against 1.5% without hematoma. Now, it's very important that we also looked at non-clinically significant hematoma, a little bit of pocket bleeding. And that wasn't associated with infection. It was only these huge, big, juicy hematomas that we don't often see these days. And these were very serious infections. You know, almost all of these patients had to have their devices extracted. The mean length of stay in hospital was 30 days. So that's lesson one. Hematomas are really bad for you. And lesson number two is never, ever, ever, ever, forevers, never, ever, ever use heparin bridging. And this is a lesson that we learned from bruise control one. You'll remember we randomized patients to heparin bridging against continued warfarin. The result was completely unequivocal. If you look in the top line here, in the continued warfarin arm, 3.5% of patients had a clinically significant hematoma, 16% with heparin bridging, so never, ever, ever, ever use heparin bridging. And all subsets showed the same result. Lesson number three comes from bruise control two, which it's actually reasonable to either briefly interrupt or continue DOAC around device surgery. So this was bruise control two. We randomized patients to either continuing their DOAC right through their surgical period against brief periods of interruption. In the continued arm, obviously, there was just what you would expect, 12 hours or 24 hours between doses. In the interrupted arm, there were 72 hours between doses. And in both arms, we found very low hematoma rates. If you remember in bruise control one, the hematoma rate with bridging heparin was 16%, with warfarin was 3.5%. With continued DOAC, it was 2.1%. With interrupted DOAC, it was 2.1%. So, you know, I think it's a patient-by-patient choice. If they're very low risk for stroke, it's quite reasonable to interrupt them. If they're very high risk for stroke, it's quite reasonable to continue them. The DOAC, if you're planning to do a cardioversion on the table, you should certainly continue the DOAC. If you're planning to do a DFT test on the table, you should certainly continue the DOACs. There's a gray area in between that's left to physician and patient judgment. And this is the fourth and final lesson for us, is that antiplatelets are important, too. Now, we've known this for some years, but what I'm going to show you someday is to show you that antiplatelets on top of oral anticoagulation is important, too. These are data that aren't published. We presented them last year. The data are under review. And what we did with this study is we put the BRUISE Control 1 database and the BRUISE Control 2 databases together. We had patient-level data. They had the same primary endpoint assessed in all patients who were able to do this quite easily. We came up with a total of 930 patients who were on no antiplatelet therapy. 408 patients were either on single or dual antiplatelet therapy at the time of the surgery. Now, the detail here is important as well. There were some patients who had temporary interruption of their plavix as part of the protocol for at least five days. Those patients who had temporary interruption of plavix, those were not counted as being on antiplatelet agent for reasons that are reasonable. And this is the bottom line. Actually, this is the wrong slide. This is the right slide here. This is the bottom line here, is that antiplatelets on top of whatever brand of anticoagulation you had roughly doubled your rate of clinically significant hematoma. So if you were on no antiplatelet agent, 4.3% risk of hematoma, 9.9% double with single. We really didn't have a lot of patients on dual antiplatelet therapy to really make much sense of this data. Only 25 patients on that. Again, the devil is in the detail. The significance was driven by the bridging heparin group. But one thing to note from these results, although the p-values are negative because of the small sample sizes, is the consistency of the antiplatelet effects. So here, if you look on the bridging heparin group, no antiplatelet agent, it roughly doubles the risk across all subsets of continued warfarin, 2.5 to 4.8, interacted NOAC 1.9 to 3. So roughly double the risk of hematoma with antiplatelet agents on board as well. So these are the four lessons that I have for you from Bruise Control 1 and 2. Hematomas are bad. Patients hate them. They're sore. They're painful. But most importantly, by far, they lead to a massively increased risk of serious device infection. There's no role for bridging ever, ever, ever. Continued or interrupted DOAC is reasonable, depending on the clinical scenario. And don't forget the antiplatelets as well. Thank you. So we'll open this paper up for questions. Seth. One of the things that I've seen to notice is that there are certain patients that are off their antiplatelet agent, they're not on Coumadin, and they bleed very easily. And so you wonder, is there something about a frailty index that would tend to predict who gets a hematoma and who doesn't? Because it doesn't seem like all protoplasms are not the same. And sometimes you do the initial incision and you just realize this is a going to be tough right from the very beginning. Yeah, you know, we did a, I'm not sure if I can get my slides back up, but we actually did a multivariable analysis, including BRUISE 1 and BRUISE 2, the whole patient level analysis. And the other predictors, I wish I could put my slides back up to show you that. Can I put my slides back up? I have to do it. It's not working. I guess while you're doing that, do you use the, what do they call that thing, the Aquamantis, or do you have any experience with that to try to reduce hematomas? No, I don't have any. I don't even know what that is. What is it? I think that's an important point, that if you have someone that's on anticoagulants and you're doing a battery change, that you should prepare, and I frequently use the Aquamantis because it covers a lot of bleeding and does a good job of drying the pathway. Especially when you have a diffuse ooze and you can't stop it. I have a question. I'm trying to find it. Yeah, it's probably the third last slide or so. Yeah. Another question? Yeah, thanks for telling people I made you bruise people, David. Thank you. It'll be a punch later. This one. But have you sub-capitalized the data? Did everyone have the same surgical technique? You know, some people are using plasma blades, some people are using diathermy to try and reduce pocket bleeding. Did everyone use the same technique? And do you think the reason that warfarin gives you a slightly higher problem is because the majority of those people had metallic valves and often ran higher INRs than you would get with the DOAC? Yeah, to answer your first question, we had some limited data. You know, it was 20 different centers and 50 different operators, so we had limited control over how they did things. Most centers in Canada can't afford the plasma blade and so on, so we just get simple cautery. We did look at sandbag use afterwards, and that didn't seem to make a difference. In bruise control 2, there was a little bit of intrapocket hemostasis agents used, and that did seem to have a small effect. But that was about all we were able to look at. What was your second question? Do you think warfarin is worse because it's often a different patient subgroup? Yeah, I don't know. Possibly. On number 2, I think the community has just gotten better at avoiding hematomas chronologically. People are just better. Most of us have got more experience. But I think number 3, you know, the DOACs bleed less than warfarin in most clinical situations. So this is, Seth, to go back to you. This was a multivariable analysis, so these were the things that popped up. Diabetes was actually slightly protective against pocket hematoma. The procedure duration increased your risk of pocket hematoma. Those were the only things. But we didn't specifically look at frailty. Yeah, thanks. Jay Schloss from Cincinnati. First off, absolutely round of applause for this trial, which shaped the way hopefully many of us in all of this practice. What I am frustrated by is, in my world at least, it doesn't seem to extend outside of electrophysiology and device implantation. So I still see people getting bridged for a right heart catheterization. I think I've seen people getting bridged or taken off their anticoagulants for things like an infusion port. I wonder if anyone else is seeing this, and can we extend the lessons that you've given us to people outside of electrophysiology? Yeah, you know, we do see that, and I see that even in my own institution, not for device therapy but in other scenarios. You know, we have the bridge trial, as you know, which was in multiple spheres. It showed no benefit of bridging over stopping. So there's multiple trials now that are in different areas of medicine that are saying the same thing. So it's knowledge translation 101. Thank you. I think we've embraced it, which I'm proud of us. Thank you, David. Thank you very much for a great talk.

pocket hematoma prevention

hematomas

infection risk

heparin bridging

DOAC therapy

device surgery

antiplatelet agents