So this is a 53-year-old smoker, one hour of chest pain prior to first medical contact. When EMS arrived, she received aspirin and a 12-lead EKG was transmitted. Those documents, the 12-leads go to the command center at Rhode Island Hospital and also to our cell phones. And so we were activated pre-hospital on her arrival. The STEMI team was already on the way in. The fellow was called down to start stabilizing the patient and consent. In this particular case, given the rapidity at which she got to the lab, she got a pressure grill in the cath lab. And we can talk about some of the preloading strategies, but that's what this patient had. Okay, so the first question I guess we can ask the panel is, you know, how many people are getting the EKGs transmitted and pre-hospital? And can we discuss the pros and the benefits of that? So what we'll do is I think for this question, we'll just go down the panel. So I'm going to start at the top just in order of how I see these pictures. So Dr. Barman, do you get an EKG transmitted to you as the interventional cardiologist and how is it transmitted? Yeah, so we do for patients that are interacting with EMS in the field. That field EKG is routed through the FDNY command center. And if it's deemed to possible or probable STEMI, the activation will go out. And it comes by way of EKG. I mean, I'm sorry, by email. So we get an email PDF that coincides with the activation. So we, you know, just log on to our email and get the EKG. So we often get the EKG before we get a call. So we don't even know that there's a STEMI other than having received the EKG. It works well. We have to turn it over every year with new fellows and new staff, but it works well. And Dr. Bortnick? Well, we're also in New York, so we have the FDNY system that Dr. Barman was talking about. However, the EKG is not only just going to our email, but it's also coming through a commercial application. So we're also able to visualize it directly on the phone and interact with the commercial application. So you can actually respond to whether you got it. You can actually text message with other individuals who have the same application. At one of our sister hospitals, we're able to do that. So there are other commercial applications that you could be using. That's fantastic. Yeah, there are some great applications, but there's one specifically that works with that particular EKG transmission. Dr. Abbott? Yeah, so we have a system called LifeNet, and it comes to our cell phone. So when you're on call, usually you have your notifications on that you've got an email. But also when it gets to the command center, they page you in case you didn't look at it. And that way we're coordinated. Great. Okay, so I think a lot of us are using the LifeNet, because that's the one you're referring to, Anna, right? Not Dr. Bortnik, right? Yes, yes. Dr. Sandoval? No, same. Not much to add, except that we do have, you know, and, you know, one of our colleagues involved in this document, Dr. Tim Henry, was very involved in many of these things. But we have a long-established, what we call Level 1 STEMI system, in which all these approaches apply. But we also do have, there's always a cardiologist on call 24-7, available to evaluate all these cases. And we'll be able to review and triage these EKGs as well. Great. And Dr. Young and Dr. Kotner? Sure. Stanford has a similar system. The pre-hospital EKG goes to three people, the attending on call, the interventional fellow, and the charge nurse. And Dr. Kahn? For us, a similar thing. So we get, the EKG gets from the fire rescue to the ED doctor, and then there's a general single activation, and everybody comes. If I want to see the EKG myself, I talk to the fellow, or I can go into EPIC and look at the EKG done in the hospital. Oh, so for you, you don't get it directly to your email? I don't get it directly to my email, no. Got it. Okay. I think we can work out to get that to you. All right. I'll keep going. Okay. Okay, so fortunately with the antiplatelet therapy in Heparin, this patient had reperfusion. And you see here, it's near Timmy III flow. She was still having ongoing chest pain. The ST segments had improved, but not resolved. And you can see here the preferred radial approach in our institution. We typically start with the culprit artery first, guiding catheter, under the majority of circumstances outside of shock. And that's something maybe we can talk at the end of the cases. But in this case, this appeared to be in line with the culprit ST elevation. So the operator proceeded with intervention. So I guess we'll stop again and maybe ask a few people. This is a large artery with an extensive plaque volume. Not a lot of visible thrombus, but with the STEMI, we know there is a lot of thrombus with the atheroma in the plaque. Can you show the picture again? Sorry. Yeah. I'm going to start by asking just one person. Dr. Barman, why don't you tell us, what would you do here? Yeah. I'll start by saying, other than the anatomy of it being a large, positively remodeled lesion, there's not a lot of features that would make me overly concerned about no reflow. And I think that's an important point that can kind of happen any time. Specifically, a very early presenter, what looks like STEMI 2, 3 flow to start the case. The fact that the STs hadn't resolved with this first angio implies maybe some antecedent, kind of de novo embolization. But I wouldn't be overly worried. I would, in this case, many cases, I would just go right to direct stenting in such a case. I would probably image here, just because of the parameters of the vessel are so kind of out of the norm, I would say, that I'd want to really understand length and diameter such that I could minimize potentially subsequent steps like post styling, etc. But, yeah, no, it's fun to see this vessel open when you get to the lab. Yeah. Terrific. Anybody here would do anything differently besides either balloon and stent or direct stent? All right. Go ahead, Dawn. Yeah, I think just to make a, not a counterpoint, I think it's a great vessel for direct stenting. But some people already have like a small balloon prepped in a wire just to kind of shut the clock off, the door to balloon time. So I think if you were to approach this with a predilation, it's more of like an undersized low pressure, shut the clock off, make sure it's dilatable, than rather taking a huge balloon in here and potentially causing no reflow early in the case. So, but in this case, what the operator chose to do was do intravascular imaging because it was such a... Dr. Abbott, can you stop for one second? Dr. Bartnick, do you have a comment? I do. And that's one thing that we brought up in the consensus statement was whether or not we should be getting a full angiogram before we proceed to the culprit. We will be talking about that. And that's definitely something that we might want to get back to here. And then to point out, there's a comment in the QA there that we should also address. Okay. Terrific. Yeah, like I said, our practice and our institution is generally go for the culprit vessel. There are exceptions to that, of course. But that was done in this case. And IVUS was done. And in this case, the vessel was direct stented. It was a 4-5 or a 5-0-30 drug-eluting stent deployed at average pressure like 12 to 14 atmospheres. You can see the positioning there with respect to the marginal branch. And then the patient basically has near asystolic arrest following that placement. Okay. So that's the point. Be ready. Be ready for the no reflow. So before you even think about what vasodilators you're going to deliver and how you're going to deliver them, you have to stabilize the patient's ABCs. This patient underwent chest compressions, epinephrine, and intubation, peripheral epinephrine. And then I guess once you've stabilized the ABCs, back to what are you going to do? So I'm going to ask Dr. Sandoval to give us his input on what is the most important step in the management of no reflow. Absolutely. So this is where I really, you know, and we worked on this document, right? It's been a disguised document now for quite some time, but I reread it today during my flight coming back to Minneapolis. And I will admit that there's a lot of information, but I guess, you know, we should all read the boxes. The boxes that Dr. Thomas-Holland mentioned, I think are really key because underscore what we need to do. And the box is clear that what we need to do is to really maximize that coronary perfusion pressure, you know, reduce LBDP, you know, give our arterial vasodilators. Which one goes first? Which one goes second? You know, I guess I can let the panel decide. But again, you're thinking here, as you pointed out, the patient's intubated, decompensated. You want to improve that pressure, reduce LBDP. You're thinking about potential mechanical or circulatory support. And again, everybody will have their favorite sort of cocktail, whether that's, you know, like hard of being a dentist, everybody can speak about different things. But again, I would really underscore that table with the key points. Terrific. One comment, because Dr. Henry, unfortunately, couldn't be on the call, but he asked me to send his sentiments. He really wanted to emphasize that in his experience and based on newer data, there is, as Dr. Abbott had already pointed out, there is definitely some evidence to show that you have potentially less no reflow with early administration of aggressive antiplatelets. And so he, you know, he wanted to emphasize the importance, even though there's the trial data is a little loose in terms of the benefits of upfront antiplatelets. In his own experience and in many of our experiences, we do see less no reflow with upfront antiplatelets. Yeah, and this case is interesting because we were so fast because of the prehospital EKG and the patient didn't get loaded until they're in the cath lab. They got a potent P2Y12 that would take effect within 30 minutes, but I'm sure that stent went in in less than 30 minutes. But given the, you know, lack of clear angiographic filling defects, I think it would be unusual for operators to have chosen to start this patient on, say, like integralin or a 2B3A inhibitor. We could ask other people, but so this is why, you know, it's not a perfect system. You're right, our data doesn't even support it, even prehospital P2Y12 maybe, but we're loading so close to the time of the procedure, and so we do need more studies for, you know, potentially these subsets of patients where maybe something intravenous would have helped, but unclear, of course. So this is just a brief cartoon to explain there are just so many factors that play into no reflow. It's not just the plaque burden, and it's the thrombus burden, and it's not just the upfront loading, but it's a lot of things like was already mentioned, the duration and extent. So we know the late presenters are generally going to have a lot more organized thrombus, and this patient was an early presenter. You know, this is a very large vessel. That is a predisposing factor. And then things like that we can't know right off the bat, like their glucose status. You know, if they come in hyperglycemic, what is their A1C? Did they get high-dose statin prior to coming to the lab? You know, we don't have time for a lot of these things, no preconditioning and some genetic variability. So these are all coming into play, and really a lot of it is outside of our control. I think the other thing I just wanted to mention, and this is an old study from what's called the dynamic registry, which a lot of us know it's a historic registry of PCI, but basically once your patient gets no reflow, it puts them in a category of high risk. Immediately they have a higher risk of shock and heart failure, reinfarction, and mortality. So, yes, the more we understand how to prevent it, the better, but there are certain cases where you just don't predict the highest risk. And if you look at all comers in STEMI and the risk is like 5% to 7% and lower, and then STEMI and very low in other situations. So, you know, again, this is just to show it's not a benign phenomenon when it happens. And, again, we talked a lot about the prevention, therapeutic anticoagulation, making sure your ACT is therapeutic, aggressive antiplatelet therapy. If you can, if your ER is going to give high-dose statin before you take them, getting acute glycemic control, direct stenting, not oversizing stents. And then there's just like a lot of other question marks, right? Like pretreatment with vasodilators, the thrombus aspiration hasn't panned out, is helping with no reflow, deferred versus immediate stenting still hasn't really been, like a practice is accepted or studied well enough to accept. Of course, deferring stenting when you don't have good flow is always recommended, but not as a routine strategy. And then once it happens, the distal delivery of different drugs, if you need to bail out with more antiplatelet therapy, LVN loading in supportive care. So we touched upon most of these. So what happened with this patient, you can see she was resuscitated. She was intubated. She had a TVP for bradycardia. Ultimately, she did have some delivery of intercoronary epi via dual lumen catheter. She was added on GPIs, and she had a balloon pump to increase her coronary perfusion pressure. Fortunately, once she regained her rhythm, she was not on any levophed or vasopressors. So a balloon pump was chosen in this case for coronary perfusion, rather than, say, something like an impella. So this just gets back to our main points about deliver those vasodilators to the distal bed and manage the coronary perfusion pressure. In this case, we achieved that with the balloon pump. And that about wraps up my case. So I'll unshare, and any additional comments can be shared by the panel. Dr. Abbott, thank you so much. That was an excellent presentation. Dr. Bortnick, I know you wanted to talk about the arterial access. We were going to talk about it later, but why don't we have you sort of tell me what you do and what are the pros and cons of each, and what is your approach? I meant to say use of the gram-versus-non-cobra. Use of the gram-versus-non-cobra. I'll tell you why sometimes it's useful, because in this scenario, for example, you see the RCA, and you go for the RCA. But with inferior MI, sometimes the culprit is the CERC, and you can be fooled. If there's severe disease in the RCA, you say, oh, there it is. But then you might notice that actually there's a culprit in the OM, and you ended up with the non-culprit vessel stented, which, you know, you'll go and deal with the other one as well. The most important thing is that you recognized it. The other thing that happens is sometimes someone has severe multivessel, and what you realize, or distal left main, what you realize is maybe you're dealing with something surgical and kind of an acute or chronic process. And so then your thinking might change, and you might decide, well, if I, for example, diurese or stabilize the patient, maybe this person really is a surgical candidate. So that's why I say, you know, look at the scenario, but think about whether or not a full endogram might help you think about the case differently. That's a great point. And, again, our document really poses not what's, you know, in a lot of these scenarios, there's no right or wrong. So I love the aspects of why you want to do a complete endogram. I generally am a component of that, but I do believe otherwise in certain situations. Anybody here not do the complete endogram first? Go up with the guide. Dr. Abbott, you just said it. Dr. Cohen, can you tell us what your rationale is and why you go up with the guide? You're on mute. You can shave off about 10 to 15 minutes, and that can make the difference. I understand that that's not a reason, but we are under lots of scrutiny when we're doing these cases because these cases get reported. Second, you know, if you have an occluded vessel, you're going to open it anyway, whatever you find in the left main. And maybe the strategy to opening it may be different. Maybe you may just do regular plain old balloon angioplasty, but most likely you're going to open it again. When the EKG is seen equivocal, I think it can be equivocal in the scenarios that Dr. Vornick mentioned, but when it's unequivocal, I think going for the culprit, going for the kill, getting it done, the patient ready, and that's fine. Then if you extend the wrong vessel, it's happened to me once, then you can do the other vessel. I mean, the complete trial and all the other trials with multivessel PCF endures that practice. I mean, whether you defer or not, that's a different topic. And finally, it's happened to me only once that there was left main disease after I extended the right. But I mean, those scenarios are very uncommon, and I think you can shave off some time by just going to the culprit. Yeah, I think there are certain circumstances like cardiogenic shock or late presentation where you just need the information. You might even be putting an MCS first, or you might be doing a right heart cath first. Like, there are certain circumstances. But, yeah, I think in 20-plus years, I think I've maybe regretted it twice in that scenario where you think the right's the culprit and there's an occluded vessel on the left and you've wasted 20 minutes. So I am extremely cautious about if there is TIMI 3 flow, shoot the other vessel under certain circumstances. So I think you just a little bit you're hedging your bets. It would be interesting to do a strategy trial to see if people's decisions would change with one strategy versus the other. But in my experience, your strategy doesn't change. It may also do with your institution because our surgeons, even if there's the severe left-sided disease, if they had a right-sided event, in most circumstances, they're going to want that patient to wait four weeks before they undergo elective surgery. And if it can't wait that long, they usually undergo second PCI. Yep. No, I agree. And I think the left trial is showing shorter balloon times in this case, but the strategy trial looking more at clinical outcomes, I think, would be important. Dr. Sandoval, I see you have a comment, and you're ready to take over for the next case. So I'll let you take over and give your comment. Yeah, we probably need to move on, but I'm just going to add a couple of very quick points. One is because thank you to Dr. Bortek for making that observation. I would say that from the document perspective, I think, and Dr. Tammies-Holland, I know that we have discussed this, is that the timing clearly, as you can hear from the panels, there's opportunity for operator preference. But they should say the complete angiography needs to be done because some people may want to just fix the culprit or maybe sometimes let's say grafts or something else and not do a full total complete angiography, whatever the timing is. So, again, a complete angiography. And the other very practical point, again, I think I like going with the guide up front, but some people could argue that let's say you have a Shepard's crook, super torturous RCA, and if you do the diagnostic first with that, then you say, like, hey, you know, pass me an AL1, a very supportive guide, so you know what you need from that information. But let's move on. So, Dr. Tammies-Holland, do you want to introduce the next speaker? Our next speaker is Dr. Selina Young, and she will be speaking to us about managing large thrombus. Is that correct? Yes, that is right. Thank you.

STEMI

EKG transmission

no-reflow

coronary perfusion

anticoagulation

cardiac emergencies