Well, I'll remind everybody again that this was a 57-year-old gentleman who presented with an out-of-hospital cardiac arrest, secondary to acute myocardigenic shock, and underwent successful revascularization with ECPALIS support, and then was admitted to the cardiac intensive care unit for further management. So subsequently in the CTICU, he was notably not having significant LB recovery, significant myocardial edema and thickening of left ventricle, despite Impella CP and ECMO. He had improvement in his biomarkers with a clearing lactate from 15 all the way down to 1.9 over a 24-hour period, but his EF was estimated to be about 20% to 25%. Thankfully enough, though, with early resuscitation and adequate hemodynamic stabilization, he was awake and following commands on day two. We quickly escalate, typically, our patients from ECPALIS with a CP to 5.5 on day two to help facilitate de-escalation of the ECMO circuit as well. Extubated on day three, and heart failure in the transplant team, we're assessing his candidacy for heart replacement therapies. He underwent percutaneous ECMO decannulation on day five successfully. He's listed for heart transplant as status 2, day 11, given his limited LB recovery with the Impella 5.5, and the thought was to facilitate some prehabilitation with an axillary device. Everything seemingly going well until he was just notably, progressively weak and deconditioned and had a prolonged ICU stay, complicated by hypoxic respiratory failure, critical illness weakness and myopathy, and unfortunately, he suffered an aspiration pneumonia from some epistaxis, small bowel obstruction, pretty similar in typical course for an Impella patient, but antibiotic therapy, gastric decompression via an NG, subsequently re-intubated on ICU day 16. That entire time, IV cangular infusion, bridging dose. This is the kind of, we're making it up as we go along. We're actually not sure what to do with that. Some of that data that you presented, Dr. Soraya, was from our institution about our PRU P2Y12 monitoring protocol, which is entirely based on pharmacokinetic data. We don't have hard clinical outcomes here, but our surgical colleagues have really leaned towards us in terms of long durations of cangular utilization to facilitate going back to the operating room for additional therapies like LVAD, heart transplant, or bypass surgery. So, we utilize this protocol based on that small single center series that we published a few years ago. Furthermore, he was considered too high risk for transplant given the re-intubation and hypoxic respiratory failure and pneumonia that he was being treated for. He underwent a bridge to transplant LVAD placement on day 23 of his ICU stay, IV cangular and heparin were restarted post-operative day 1 after delayed sternal closure, extubated on post-op day 3, that's ICU day 26, transitioned to clopidogrel and warfarin dual therapy post-op day 3, and eventually discharged to inpatient rehab on day 35. But very long ICU course, not uncommon to hear about in this patient population, but that's the remainder of his case. I may open up, I think there's a lot of discussion, a lot of questions. I certainly have a bunch. I think, Alex Struisbeil, are you in the, maybe if you could talk about your ECMO, any platelet strategies, I'd love to hear a little bit more about that. Yeah, I'd be curious, the panel, I'd be curious in the room too, I don't think there's any consensus, right? And I think there's a lot of people involved in ECMO who think just the whole circuit destroys platelets and is an anti-platelet therapy in and of itself. So we actually did a before and after study at our institution. We had a lot of CNS bleeds, we had a lot of bleeding events, didn't matter whether it was dual anti-platelet therapy, cangulor. So for our last 35 ECMO runs with PCI, either PCI pre-ECMO, PCI on ECMO, aspirin only. And we've had, so our bleeding events went way down, we've had no stent thrombosis, this is just presented by my critical care colleagues at CHESS in Boston last week or week before, whenever. And so hopefully the full manuscript out next year. So it's just interesting, and I spoke to some of your PM colleagues about this, and several of them have unpublished series, which now they want to stay, they want to publish, because I think there's a number of places that's been doing that. But I think looking at all these protocols, it's interesting, we're all over the map. And so I don't know if you guys have answers, have thoughts, but for us, with ECMO, I don't know what the answer is in repellent, but just on the ECMO, cangulor, dual anti-platelet therapy, lots of bad bleeding and lots of head bleeding, and aspirin only made that better with, so far, in 35 consecutive patients at no cost of stent thrombosis. And you use heparin with that? Correct, yeah, heparin. Yeah, so everybody's on heparin as well. And any PR, have you guys gotten PRU data alongside, because that would be fascinating to sort of know what it looks like while they're on ECMO. No, I mean, I think we, so selectively, because if some are getting it because they were on anti-platelet before, but no, on the aspirin only, and I don't know offhand what the platelet levels, the numbers, but we weren't, by intent, doing PRUs, this was sort of retrospective after we just made a clinical change, but. That's fascinating, I think what's really needed, particularly in the shock population, is more of a PRU-based study, and certainly our protocol, at least, for ECMO patients is similar to what was shown, to try to get the certain PRU level. So really, our bridge dose, I sort of laugh sometimes, bridge dose may be .5, it's whatever, sort of, you're kind of doing this to try to minimize bleeding, but also get these patients through. Curious, any other thoughts about ECMO or Impella and how you're doing? Well, no, I think, to be frank about it, it's all pharmacokinetic data, and so to Alex's point about the ischemic events versus bleeding events, we're seeing reductions in bleeding when you reduce your antiplatelet and anticoagulation, which makes sense. But the question we haven't answered yet is, what are these ischemic events in patients who just underwent a left main decay crush? Do they get stent thrombosis if you stop their P2Y12 inhibitor? And I think that's where pooling of the data, the KMO registry analysis, will garner some additional insights, but it's going to be hard to get randomized evidence in this cohort of patients, I think, because, frankly, we're all making it up as we go along. I noticed in your last slide that you continued antiplatelet therapy even when you knew the patient was heading toward LVAD, and you also continued to postoperatively. That's not something we normally do. Normally, when we know the patient's heading for surgery and there's no chance of recovery, we stop antiplatelets to limit bleeding events because we know the heart is gone, and we actually take out the vents and just keep the patient on ECMO. But I'm curious to hear your experience with that. Yeah, and that's a lot of anecdotal experience there. We had a few cases of left main stent thrombosis and ventricular tachycardia after escalation to durable VAD. So our heart failure cardiologists have been a little bit queasy about stopping their second antiplatelet therapy, and that's why immediately when safe postoperatively, we've gone back on Kangalore. But again, data-free in that regard. It's purely anecdotal. Respect to your surgeons. Any other thoughts there? All right, so I've got a question. So for the audience, how many people have Kangalore? or on formulary at their hospital. Okay, and then my next question, so a shock patient comes in, they're in the cath lab, they're getting PCI, how many hospitals, or how many of you in the majority of times are just using oral or any platelet therapies in shock? Okay, how about cangrelor? And then how about epifibatide or other GTBs? Yeah, I think still a lot of, decent amount of GTB3A inhibitors still being used. It's sort of being seen as interchangeably. I think the concerns there with that agent in particular is renal dysfunction often unfortunately occurs concomitantly with these cardiogenic shock patients, and we know that epifibatide really builds up quite a bit. And then next question for cangrelor, how many run it at the PCI dose and then go to bridge dose, versus just running the PCI dose? What's sort of the split? So PCI to bridge, first off? And then how many are just running the bridge dose subsequently? Okay, and is there, and would you say that if anybody's willing to speak out, is there sort of different definitions of bridge dose at your institution, or is it pretty much 0.75, or sort of doing the 0.5, 0.4? Okay, okay, all right. Any other questions from the audience? I think in talking to a lot of people and the hesitation in using cangrelor, a lot of times comes down to cost. Cangrelor costs more money, and so there's been hesitation, I think, initially to start people on it and then keep them on the cangrelor for long periods of time. I will mention that there was a study that came out recently that looked at the use of cangrelor, increasing the use of cangrelor and what that does to hospital costs. And actually it showed that when they increased the use of cangrelor from 11 to like 32% in their patients, they reduced their ischemic events by about 6%. Bleeding did go up by about 2%, but overall hospital costs actually decreased by 12%. And a lot of that is because of reduction of ischemic events, lower length of stay because of bridging to LVAD or transplant if needed, and lower use of 2A, 3B inhibitors, things like that. And so I think just from a, when I get resistance from people, if I wanna start cangrelor and they tell me about the cost, I think I just present them that information and the right patient, I think it's worth it and will save costs overall. All right, we've got a question. Yes, regarding the antiplatelets, there are, I think you say dual antiplatelets. We're talking most of the time P2Y12 inhibitors. What about the IV aspirin in this area? I would say we don't, I'm not sure of any of the rest of you guys, we don't really use IV aspirin. I think even in patients that can't take it orally, either give it rectally or down the tube, so not a whole lot of experience with IV aspirin. Hi, I have a question about platelet reactivity testing. It sounds like your centers are using it for cangrelor titration, but in other instances, are you routinely checking platelet reactivity assays or only when there's a clinical concern for inappropriate platelet inhibition? The only time I, at least in my institution, that we're using it is prior to surgery or in our ECMO patients. That's the only time I see it when we're on a long-term cangrelor to make sure we're at adequate PRU levels. But otherwise, I think in the past, it was used quite frequently to determine some P2Y12 inhibitor resistance and things like that. We don't do that anymore. What about you? Yeah, we do the same. We use PRU testing only preoperatively to make sure that the antiplatelet has washed out before they take to the operating room. We need to take some surgeons from your institution to ours, but other than that, we don't use it from ECMO. I actually took a picture of your slide. I don't know if you can see. It feels really great to see pictures of your slides taken. I took a picture of your PRU titration. Yeah, our MCS utilization has led to us using PRUs to see if we can de-escalate the dosage to reduce or minimize some bleeding events, but yeah. And then I think maybe I'll ask the panelists this question. I think I oftentimes struggle. So I had a patient the other night coming in, obvious big inferior STEMI, in shock, put RPFlex in, stabilizing the patient out, intubated, sedated, actively was vomiting before the procedure. Gets internal access in our ICU. I start on Kangrelor during the procedure. At what point do you feel comfortable and confident of putting Ticag down the tube? What's sort of your decision or pivot point about how to do that in your ICU? So ours is pretty straightforward that we don't. Anyone on mechanical support or inotrope dependent after an AMI, we continue Kangrelor until the inotropes are weaned, but I'll have others comment too. No, similar thought process and approach there, and I think kind of similar analogies we use in the ICU setting. We don't typically think early internal nutrition on a patient who's on multiple vasopressors and mechanically ventilated is gonna adequately absorb that. So I have some hesitation going directly to an oral antiplatelet therapy, thinking that there's gonna be legitimate absorption there. So we'll use the bridge dose Kangrelor to get over the hump for the next day or two in the ICU to help facilitate extubation, decreased pressure requirements and whatnot. But that's where that falls in. Yeah, I think we just, when you have, when the patient stops essentially vomiting, putting an OG tube down and suctioning all of those contents or stabilizing that, it might take a day or so, but then I think after that has been stable, and when you feel like you're comfortable feeding them, then I think I feel comfortable switching to an oral agent, and that's what we've done. I think the other thing about internal nutrition is in a lot of these patients, I think we escalate internal nutrition very quickly, and then that results in aspiration events in our patients. So we go from 10 to 40 within the first four hours. What I've done is actually keep them at the trickle feeds for like seven days. That's actually been shown not to decrease nutrition or protein in patients. So you get the same amount of benefit from just keeping them on trickle feeds for those seven days, but then you reduce aspiration events significantly. And so I've taken the strategy of just leaving people on small feeds, and that reduces how many times they vomit or aspirate. For trombocytopenia, how do you differentiate between tromb, inflammation, and heparin-induced trombocytopenia? How do you manage? Or just switch heparin to bivalvegal gluten? Yeah, it's a very difficult thing to manage, I think. I mean, usually there's such significant hemolysis that it's pretty rarely hit, and I don't know, I feel like it's a fatal diagnosis for these patients to get hit, so I try and not look for it unless I really, really have to. But the only times that I really do look for it is when the platelet count is out of proportion to the amount of hemoglobin that's being lost, and the hemolysis markers, then I'll start to think about it. Our surgeons actually routinely use bivalveglutin for this reason on all MCS patients, to just take that possibility off the table. But that's not something we've done, but I'll ask others. We all have a very similar thought process there. I think we overestimate the diagnosis of hit in the ICUs in patients who are on mechanical support or in cardiogenic shock. There are some institutions that are just going to a bivalve first strategy because if it does ever become hit, then that minimizes the risk of any of the issues there. But there are always multiple ideologies of thrombocytopenia in contemporary ICU patients, so it's hard to really tease that out as a mechanism of an autoimmune phenomenon there. Sometimes we do the same for anti-platelet factor four, but it came back later, maybe seven days later. Yeah, and that's the difficulty there because if you plug in four T-scores in a lot of these patients, they will always be intermediate, which the next steps will be to send the PF4s and the SRAs, and so overestimated diagnosis. So to transition just a little bit, but I wanted to get some thoughts because I think this is just kind of a fascinating area with bypass, with patients undergoing bypass. So patients coming in, maybe with acute myocardial infarction, unstable disease. Maybe we're on a P2Y12 inhibitor going into the cath lab, maybe not. What's your general strategy at your institutions? I think it's really variable around the country. Are you okay with just washing out the P2Y12 inhibitor? What scenarios would you not be going into CABG, and when are you using Kangrelor and proceeding CABG? Do you want to go backwards so you're not blindfolded? So it's what the surgeons, you know, what the surgeons want. So a lot of times they'll want, you know, a three to five day washout period of P2Y12 inhibitors, and so we'll do that. You know, we'll switch them to Kangrelor and give them that washout period and then go from there. Yeah, it's entirely dependent on which surgeon is on call and who takes the call when we call. Yeah, I think that's the theme. We normally do IV Kangrelor and then turn it off six hours pre-surgery, and there's some people who check a PRU, there's some people who don't. There's some people who still believe Kangrelor is voodoo and just use heparin and no antiplatelet therapy just so they can turn it off, but another area that I think practice is highly variable. Yeah, we're all over the place. There were some Bridgestones, some say you don't need anything, just wash out the oral P2, they'll be okay. Some are using occasional boluses of eptafibatide. It's really, really highly variable, so I think an area for opportunity to understand more consistency in practice. Did want to bring up, you talked about a couple of trials coming down the pike with Saladigrel, so we've been pretty involved at the DCRI for SOSAMI, and many of you may be actually sites in that trial. That is a subcutaneous injectable P2Y12 inhibitor, fast-acting thoughts, that is when the patient has had a prior MI, you give them Saladigrel, and essentially it's like the EpiPen for the heart attack. They carry it around with them, they inject it at recurrent signs of chest pain. The biggest issue we have is, what percentage do you think, is anybody willing to guess, of all the patients, and we've enrolled maybe 4,000 at this point, will inject with chest pain that's bad enough to call 911? Anybody guess? About 4%, so people are not thinking about injecting, so that's been a major limitation to that trial, and I think will be tough going forward. With the injectable GTB3A inhibitor, I think also interesting to try to potentially abort a really huge heart attack from occurring with big thrombus burden. Biggest issue is, in order to really make that work, you need to have EMS's ability to stock the GTB3A on their trucks, and that's been difficult in that trial in the U.S., it's primarily being done in Europe right now. So I think trials coming down the road that may have some new findings, but I think a lot of logistical barriers in some of those trials, but interesting nonetheless. All right, I think we're almost at time, so I think there's a breakout session maybe that we're going to next, is that correct? Yes. All right guys, so we have about a 15 minute break. There are three breakout rooms just above us. The three breakout rooms are gonna be, one is essentially geared towards the cath lab and cath lab technicians and nurses. The second breakout room is an intensive care breakout room and the third one is related to shock coordinators. So we have a very multidisciplinary group of people within this room, so you can feel free to learn something new, go hang out with your friends, whatever you prefer, but we'll start those sessions in about 15 minutes, we'll clear this room so we can clean up after lunch, and then after that session is done, we'll all join and finish out a couple more sessions in this room, so thanks. Thank you.

cardiac arrest

cardiogenic shock

LVAD placement

antiplatelet therapy

ECMO complications

injectable therapies