On the topic of this never happens, this happened Thursday. So let's dive into it. We'll present the case, and hopefully it will prompt some discussion about options both to prevent this and to deal with it after it happens. This is an 80-year-old gentleman. He came in. He had really no medical follow-up before, God bless, at 80 years old. Came in with chest pain, came in with dyspnea that was somewhat staggered and fluctuating over three days. As you can see, he was fairly benign, T waves a little bit flat. His first reponent was 0.06. He got started on aspirin. He got started on a heparin drip. He was scheduled for coronary angiography the next morning. He had this kind of mild troponin elevation, and then it came down. But then the morning of the procedure, he was scheduled for noon, and he started having this fluctuating chest pain in and out again. No ST elevation on EKG, but he was one of these scheduled for noon, having chest pain on the floor, bumped him up to the 7 a.m. case. He'd had an echo done when he first came in. He had some mild infrared wall hypokinesis, up 45% to 50%. So per usual, radial access, we shoot the left side, nothing crazy, calcified, kind of mid-LAD disease, nothing terrible. So he had kind of this ectatic right coronary artery, Timmy III flow throughout, but certainly diffuse mild to moderate, some sort of ectasia and disease, and there was this lesion up top, which when you first glance at it, you say, I don't know how terrible it is, but it's bad. When you really look at it, there's a cleft in it. It's ulcerated. It's just terrible looking, and it's sitting inside a true kind of ectatic artery. So we said, okay, this guy, he's 80. He's got some LAD disease, but it's certainly not terrible. He keeps having this chest pain on the floor. This is someone we certainly want to do everything about. He's got his aspirin. He's on his heparin upstairs. We're going to go ahead and fix this thing. It also matches up with that infrared wall hypokinesis. So we put a guy down. We put a wire down. He's heparinized in the lab. We do a little bit of balloon angioplasty, just a 3-0-15, a merge, in part just to get an IVAS catheter down and across. And so then we IVAS. You can see we've still got Timmy III flow through that whole area. We find like the one healthy segment in the artery, somewhere in the mid-to-distal segment. It's like this is probably a pretty reasonable place to drop down a pretty big stent. We put a 4-0-38. So we're certainly not small distally. It's not like we're dropping a 2-5 and a 6. Put a 4-0-38 Zion SkyPoint across both the distal lesion and then kind of the proximal lesion, not all the way back to the ostia, but we're going to get there with the second stent is the plan. And we do it. Stent's up. We take a little puff. Look at us. A little bit slower flow, but I'd still probably call it Timmy III. You know, we're undersized a little bit proximally. We've got some work to do, but not a bad kind of distal size for our distal stent edge. And we post-dilate. We go up with a 4-5-20 NC balloon. We post-dilate it serially, and then there we are. So we've all kind of been there, and in this situation, if you look close, you kind of see this mobile stuff moving around in the proximal part of the stent. At this point, he's chest pain-free, but this happened three seconds ago. At this point, his heart rate's 70 and his blood pressure's 150 over 88. At this point, his ACT was 240. And I think that's our pause point to discuss the case. All right. Great one. We have all been here. I was going to ask you about it. So this was done on heparin. Yep. And the ACT, you did it at this moment, right? ACT was like coming back at this return. So we'd drawn an ACT, and then, you know, the first question when you hear the beep and you see this is, what's the ACT? And someone says 240. And the patient was on aspirin? The patient had gotten a full aspirin when he first came in, and then an 81 the morning of the procedure. All right. So let's start. Dr. Geary, tell us what you think about this patient and what you would do. So, again, anticoagulation with mono-antiplatelet therapy, but that is fully loaded on the aspirin. So what we have here, obviously, is proximal acute stent thrombosis, which is surprising, I would say, based on the series of events. I was not expecting it, except for the fact that the talk was titled that, because we have four-host stent, but it seemed like an easy case, four or five posts still. Whenever I have had this happen, I've got a checklist that I go through in my mind, and I try to just hit them all very quickly. Things are often happening in parallel. First thing is antithrombotic strategy. So we're always judging antithrombotic strategy with risk of thrombus versus risk of bleeding. Here, that is a known risk that's sitting in front of you that's already realized versus very theoretical risks. You're going to throw the book at the patient. He unfortunately hasn't had a P2Y12 yet. So this is obviously a super appropriate place to start Kangalore as your P2Y12. And despite that commentary on 2B3As, which I think is well-warranted, I would 100% also bolesome with the 2B3A. I mean, it's a potentially catastrophic situation right here. The second issue is, is there a role for thrombectomy catheters is my next step that I start to think through in this case. There's pros and cons to them, as we all know, and there are different versions of them. Typical aspiration thrombectomy versus kind of mechanized aspiration. Issues with them that have emerged is sometimes, despite what you're trying to accomplish, you could sometimes lead to more clot embolization because the device lumen may not be quite large enough to accommodate something that's 4 or 4.5 where the thrombus is forming. But it may. It's just hard to say. So you're always guessing a little bit. There's a theoretical risk of stroke, which wouldn't be high in my mind in that decision-making right now. I'm more worried about just sending this into a place that's going to be even potentially harder to deal with downstream. And then the third issue is that I'm thinking about is if we end up doing these things of getting the meds in, performing thrombectomy plus minus angioplasty, what do we do if the no reflow actually happens? And with that, I'm thinking about drug delivery issues into the microcirculation, which I'll usually perform with a dual-lumen catheter. So you maintain your wire position, send a dual-lumen catheter down, and inject through the rear end port of the dual-lumen catheter, vasodilators, plus or minus epinephrine. And then finally, because it's a large dominant right, there's a chance the patient's getting very sick on you over the course of the next like 3 to 10 minutes, potentially even going into cardiogenic shock. It's unfortunately probably going to be a biventricular shock phenomenon with a huge inferior problem plus an RV problem. But I'm also heavily considering in parallel fashion getting groin access, at least at minimum with the placeholder sheet, and having somebody bring in support devices into the room in case I need to crash onto them emergently. I'm asking for another attendee to come into the room if I'm lucky enough this is happening during the day as well to be a second cloud of hands. Yeah, there's a lot to discuss here, and Jay went through a lot of the points. One of the things that we talk about is that there's a multitude of factors that go into stent thrombosis, and in this case, though, it feels fairly likelihood that this is a lack of a P2Y12 or perhaps a second P2Y12 agent, just given the fact that you were pretty big with the stent and you had guided your landing zones accordingly. For me, my practice is usually, particularly in an 80-year-old, to just preload beforehand. But that being said, I probably would have preloaded him with Plavix when he came in, just given, again, the fact that he's 80. And so who knows if he has a genetic polymorphism or whatnot, and perhaps it wasn't effective enough. So it could have still been in this position. I think my move here, given the fact that in this particular case, I think it would have been due to the lack of the P2Y12 inhibitor, would be initially Kangalore. And I agree that, you know, in regards to the comments made about aspiration, this is not our usual go-to, but in this particular case, I'm putting a mechanical aspiration catheter down as the Kangalore is getting started. I think I would then wait, see whether or not I needed to give an additional 2b3a inhibitor or something else. Perhaps those two things alone, starting Kangalore and mechanical aspiration, would do that. And I love your comments about dealing with the no flow or the slow reflow, you know, maintaining wire position through a manual aspiration catheter and still being able to deliver drugs distally, including epinephrine, is huge in this case. Knowing that concept of being able to pull epinephrine from the cold cart, you take 1cc from that, dilute it into another 10cc syringe of saline, and then give 1cc of that into the coronaries, will really…has been very effective in significant slow flow, no reflow cases. Yeah, and I agree with all that. This looks like probably a lot of distal embolization, a big thrombus burden that went down, which is funny because we didn't see that much thrombus in the initial lesion. It's just a…it's an angry plaque, essentially. I'm curious about the…sometimes the timing helps. So we have to do a lot of things in order to assess the patient. We have to treat the anti…platelet therapy, anticoagulation therapy. We also have to see if that's going to have an effect. So I'm curious, will everybody…I would also do the Kangalore and then wait on the 2b3a and see after aspiration if it gets better because you have to give it some time as well. The other thing is sometimes the ACT comes back high, and the first one's not accurate because maybe you drew it from something that had heparin in it, and you don't really know. And so I oftentimes repeat it, and the next one is like 180. I'm like, oh, man, that's something else. So you could also give another bolus of heparin at the same time just to cover your bases as well as the Kangalore. So you make sure and do that, like Megha said, ourselves, intra-arterial so that we know that it's getting in because sometimes I've also had that the IV is infiltrated by then or something like that. So… Or disconnected and things are… Or disconnected. Although it is high, but yeah, exactly. So who would give a 2b3a inhibitor at the same time as Kangalore? It sounds like Jay's doing that. How about the others on our panel? And then… I wouldn't. We were talking about this just a few weeks ago, and I think our 2b3a use is almost nonexistent now in the lab with Kangalore. So typically if I give this, the only other two things I'd add is I'd probably run an IVS catheter down and make sure that the proximal edge looks fine, which I'm sure it does. But just with that haziness, make sure there's not some other obvious cause of what's going on here. And then I completely agree with what Jay was saying about support, and I'd probably have the fellows start working on getting a right heart cath up just so that I have an assessment. And if the patient's sick and doing okay and everything starts working, then I try to avoid it. Now let's say, you know, he's obviously in shock and, you know, going down quicker than at that point, maybe consider the 2b3a, but I haven't used it in this case. I find that when you're doing the right heart and maybe the balloon pump or whatever you want to put in, then you come back three minutes later, it might be so much better because you have to get the agents to get in the system and to percolate there and to have their…to work. And I think what Vinita said about epi is that's been really a game changer in these sorts of cases. Nadia, any thoughts? Yeah, no, I was just going to say that I probably would wait on the 2b3a inhibitor myself in an 80-year-old patient just to see if maybe give it a couple minutes, especially because it takes effect quickly and just…I know we already talked about the heparin being unreliable. Those ACT machines also have plus or minus 30, so like, you know, if you have drawn it from some place where there's a little bit of extra heparin and then plus the machine is plus minus, it's just very difficult to rely on heparin alone. The other thing is the radial case, but in the old days when we were doing more femoral and now you're going to add a femoral for the mechanical support, that's where the 2b3a tends to blow up. It tends to be the groin axis and then you have to deal with that. Not that it happens every case. It's still probably less than 1 to 2%, but it's something else that you have to worry about. But certainly if you need to, it's not improving despite all your efforts, then you have to add more therapy. And I think that then a 2b3a bolus and or a drip would be relevant there. Any questions from the audience? I mean, well, consider also the distal library, the blood pressure is strong, at least right now. So that's another thing you can do on that. You can get the catheter down, you can inject the lenipride and also use the same catheter for the aspiration. That can work well. I was curious to see how it turns out, because I'd be very surprised if there's not an element of no reflow already. I know with a filling defect approximately, you can't say no reflow because it's not a normal artery, but I'm suspicious that there's no reflow, I'm curious to see. How many are giving nipride routinely pre-aspiration? I do. I, you know, unless they're really, really hypotensive, I give nipride routinely before I start aspirating in case for the no reflow situation. And you bring up a good point about the blood pressure for this. I probably wouldn't give epi if the pressure's already high. Be careful with the blood pressure, because sometimes when stuff hits the fan, the blood pressure goes up first before they crash, right, because they have the adrenaline rush. So sometimes you have the nipride, then all of a sudden everything's crapped. Look at pulse pressure. That's really important. Pulse pressure is more important than the systolic blood pressure.

chest pain

dyspnea

coronary angiography

stent placement

acute stent thrombosis