CHIP Part 4 Acute Coronary Syndromes - Coronary Track - CVI 2023

All right, we're gonna get started because, and so, this is a cool format, and um, we have a lot of really good stuff to talk about today. So I am Tim Henry from Cincinnati Christ Hospital, and my fellow moderator is Bonita Shaw, uh, from New York City. And we have a great group. I'm going to introduce people as we go. Our first talk is going to be 10 minutes, talking about year in review of like highlights in ACS. So this is a session about acute clearing syndromes, and we have some really good cases. But Rajiv is going to start us with data that we need to know. He gets 10 minutes, and we have time for discussion.

Thanks Tim. Thanks Bonita. There's a title up there, so year in review, no disclosures, three trials in 10 minutes. So I'm going to ask for a show of hands for three questions on each of the studies. A 73-year-old male with an inferior STEMI presenting within two hours, and he is 75 minutes from the PCI center from your Center. So we'll have the answers are up here. Here, hands up for lytics and transfer. That's a pharmaco-invasive approach; you give the lytics and you plan transfer. Hands up for number one? Okay. It, hands up for number two, transfer for primary PCI. Okay. Well, now the first trial to talk about is the STREAM-2 trial. This is only just out, and there's a title. This is half-dose TNK or primary PCI, and the TNK is as part of a pharmaco-invested strategy in older patients with STEMI, randomized open-label trials. So a background, a really important study, the STREAM trial is now a decade old, and that established a role for pharmaco-invasive strategy; that means lytics and then transfer for PCI between three and 24 hours, or if you don't re-perfuse to get rescue PCI. And you'll see here that the pharmaco-invasive strategy actually had numerically better outcomes than primary PCI, driven by fewer reinfarctions. Two-thirds of patients reperfuse with the TNK bolus early in the trial. It was observed there was an excess of intracerebral hemorrhages in the elderly, and so 20% of the way into enrollment, the protocol was changed to half-dose TNK, and there were no hemorrhages in the next 97 patients. So this led to the study question we're talking about now: Is half-dose TNK an effective and safe strategy for pharmaco-invasive in older patients 60 years older presenting with the STEMI within three hours and unable to get pPCI within one hour? So here's the study design: 400, two-to-one randomization, pharmaco-invasive, you can see the pharmacology here, antiplatelet and an oxaparin versus standard practice pharmacology for primary PCI. Mean age 71, anterior MI and 43, and just like the STREAM trial, about 33, 34 did not reperfuse with a half-dose lytics and needed to have rescue PCI. Well, the primary endpoint you'll see is death, heart failure, MI, and shock at 30 days. There was is no difference between this half-dose pharmaco-invasive strategy and primary PCI. Symptom to reperfusion times are over there, just so you know. The time to lytics from randomization was 10.1 minutes; the time to sheath in was 81 minutes. So actually, if you think about it, that's not that long. This is not patients who are hours and hours away; it's a relatively quick transfer for PCI. Some more numbers here: The final TIMI 3 flow was the same in both groups, as was all-cause and cardiovascular mortality. The key finding, I think, for this study is that intracranial hemorrhages was still there: 1.5% in the lytic group, even the half-dose, and zero in the PCI group. And of the six patients that had hemorrhage, all were under 75, half were fatal, and two of the fatal actually had over-anticoagulation, meaning that they had the enoxaparin, aspirin, and Plavix, and then a full dose of Heparin at the time of rescue PCI. So whether that played into this remains to be seen. But as an important caveat of the study. So the conclusion of this trial, according to the investigators, was having the dose of TNK in a pharmaco-invasive strategy in this early-presenting STEMI population was associated with similar outcomes and ECG changes, a higher risk of intracranial hemorrhage, and they conclude that if timely PCI is unavailable, then this half-dose strategy is a reasonable alternative to pPCI. My commentary is that this was a disappointing trial. This has not advanced the needle for pharmaco-invasive strategy, this, for two reasons: Number one, there was no signal for an ischemic benefit. You'd hope that immediate lytics, even half-dose, might give a signal for a better escaping benefit, just like it did in STREAM, but it did not in this study, with a caveat that the median time to pPCI was only 81 minutes. So, as I said, this is not patients from many hours away; this is a relatively close transfer. The second disappointment was the excess of intracranial hemorrhages. So, in italics, the existing pharmaco-invasive setups could move to half-dose of TNK; that seems reasonable based on this trial, but I don't think this trial will move the needle in places that already have primary PCI in their networks.

The second trial. All right, a case. I'm going to have a show of hands again. 65-year-old, one year after PCI to mid LAD for non-STEMI with moderate disease, conservative therapy, and average ischemic and bleeding risk. So this is a secondary prevention question for long-term secondary prevention. What monotherapy do you advise? Hands up for aspirin, and hands up for a P2Y12 inhibitor. Okay, so that's the the question here. This is a meta-analysis just published, uh, this month, uh, looking at that question. And the background here is, uh, we know that lifelong aspirin monotherapy is still standard of care after DAPT. We've had randomized trials, most recently the HOST-EXAM trial that looks at clopidogrel versus aspirin, others that have looked at ticagrelor versus aspirin in a variety of atherosclerotic populations, but no prior meta-analysis that studied just patients with CAD. So the study question is: P2Y12 inhibitor or aspirin monotherapy for secondary prevention and established coronary disease? Here's the methodology: Seven randomized trials, mostly with clopidogrel. The primary epic efficacy outcome is ischemic, and you can see that there the key secondary outcomes of major bleeding and net adverse cardiovascular events. And a one-step meta-analysis, ischemic endpoints, P2Y12 inhibitors were better than aspirin over two years. So fewer CV death, MI, and stroke, again driven by reinfarction, and you can see that in the estimates down here. Bleeding, actually also P2Y12 were non-significantly better than aspirin over two years. You can see the strong trend toward a benefit of P2Y12 inhibitors, and the net adverse events again, P2Y12 inhibitor was the winner, driven by fewer ischemic events compared with aspirin and a trend toward less major bleeding over two years. So the P2Y12 inhibitor was the winner in this meta-analysis, and that's the conclusion here is that given the superior efficacy and similar overall safety, the P2Y12 inhibited monotherapy might be preferred over aspirin and monotherapy for long-term secondary prevention in patients with established CAD. My commentary: I got the podium; I'm able to give a commentary. I think this is another nail in the aspirin coffin. Ashwin, we know is now not useful for primary prevention; we no longer use triple therapy. But the question is pragmatic. I think: Are we really going to have our patients on P2Y12 inhibitors only? So what if our patient two years out after a stent needs a a knee replacement? Are we going to now be happy for them to stop that Plavix, because that's what the surgeon is going to want to do? Are we going to bridge them with aspirin? Is this a new problem we're creating for ourselves? We'll see. So I think, despite the finding of this trial, I think it's going to be a struggle to change that perception of the safety of a baby aspirin, safety of a baby aspirin, despite what the data shows for secondary prevention.

The third and final trial is the case again for a show of hands. 58-year-old male with an inferior STEMI, radial access, and the plan is a contemporary PTCA, drug-eluting stent, and IVUS guidance. Dual antiplatelets are on board, and no plans for routine glycoprotein inhibitor therapy. So the question for you: three options regarding the periprocedural antithrombotic. Hands up who uses who uses bivalirudin? A few there. Hands up who uses unfractionated heparin, but will be open to persuasion with a trial I'm about to show you? All right, and hands up for who uses heparin and no matter what they're not going back? Okay. All right. So this is the BRIGHT-4 trial, published in The Lancet in November. Um, we'll do some brief background on bivalirudin. Um, many of you will remember and still be scarred by some of the trials that we've lived through over the years. But in brief, HORIZONS-AMI, bivalirudin was the winner, but it was a super controversial study, was followed by the HEAT-PPCI study from the UK, whereby bivalirudin was not better, and there was a four times risk of stent thrombosis, but there was no post-PCI infusion of bivalirudin. So then comes a MATRIX trial, and that showed that there was no benefit to prolonged bivalirudin infusion. But remember, from that trial, the clinicians had the option to use a low-dose prolonged infusion, 0.25 milligrams, or the high dose, 1.75, and the post-hoc analysis suggested that the best outcomes in the whole trial were in the group that had the higher dose prolonged infusion, the 1.75, post-hoc, etc. But that led to this study question: Is bivalirudin plus a prolonged full-dose infusion in STEMI superior to heparin in reducing mortality and major bleeding at 30 days? Here's the trial: Lots of patients, right? Three thousand in each group. There are the numbers. This is the high dose over here, 1.75 for two to four hours. If the ACT was less than 225, you got an additional bolus of bivalirudin or an additional bolus of heparin. This was a contemporary study, radial, ticagrelor, restrictive GPI use. Some caveats: This was only in a single country, and it was, of course, open label. So here are the findings: The primary outcome favored bivalirudin, all-cause bleeding, all BARC 3 to 5 bleeding being the primary outcome measure. Now, 1.3 absolute risk reduction, has a ratio of 0.69, and also the secondary outcomes in general also favored bivalirudin, all-cause mortality, stent thrombosis. This is wild; all the other studies showed more stent thrombosis with bivalirudin, yet this high-dose infusion shows a statistically significant lower dosage than thrombosis, bleeding lower as well, but no difference in reinfarction, revascularization, and stroke. So the conclusions here, uh, the interpretation was that in patients with STEMI undergoing primary PCI in the contemporary era, anticoagulation with bivalirudin plus a high-dose prolonged infusion reduced the composite of mortality or bleeding compared with heparin. Well, gosh. So my commentary here is: This is certainly provocative. Is it possible that just that change in the dose of the infusion swings your stent thrombosis from an excess risk to suddenly a protective risk? Well, that's certainly very provocative and worthy of discussion. I think the limitations of this being open label and a single country are serious, and for many it will not change their practice. I think most will stick with unfractionated heparin. And oh my goodness, yes, it is true; more randomized trials are underway. So with that, I think I've finished in eight minutes, 50 seconds. Here are your three findings: Pharmaco-invasive did not beat pPCI in the elderly; P2Y12 inhibitor was the winner for secondary prevention; and bivalirudin, that pendulum is swinging back in. Thank you.

All right, Dr. Galati, great job. Enzo, Bonita, we're making this up as we go. So how about this: We get five minutes, you get five minutes, and I'll introduce my panelists and you do that. So, so I'm going to ask everybody a question: How many in this room have even used a thrombolytic? So less than probably a quarter for sure. So I think in one comment I'd make about the STREAM data is, um, disappointing. I think the bleeding issue was due to over-anticoagulation, and the second comment I'll make is, um, if you look at patients that are transferred for STEMI in the United States, so more farther away, more than 70% are being treated in greater than 120 minutes. So this is a huge problem, and so I think look carefully at the pharmaco-invasive because I think in the right patient population there's clearly a role. So now I'm going to introduce my panelists, and you get one comment or two, and uh, so first of all, uh, summon our aim, and then Mega Prasad, and then Jacqueline on Thomas. Oh, introduce myself. Yeah. Oh, make comments about those great people. Oh, wonderful. So, so excellent talk, you know, to do it within 10 minutes, it's amazing. So you know, I actually am an interventional cardiologist in Houston, uh, the Texas Medical Center. We have a pretty big network of, uh, you know, um, sort of Life Flight and patients coming for an MI. The program was set up about a few years ago, actually a few decades ago by Richard Smalling, and he's a big believer in in half-dose. So in the HFD system, we actually use half-dose slices frequently, even before, based on the STREAM trial. And so we do, um, have those rather plays, and I don't, and obviously this is recall bias, I don't recall seeing a lot of intracranial hemorrhages. We've often talked about going back to HFD and getting the data, but my feeling is it's probably safe, but is it better in this older population? I think the data still needs to come out, but we use it frequently for our patients who get transferred, and sometimes these are patients who are transferred from within Houston because of the traffic, it takes them that long to get to our lab.

Jacqueline, we want to follow that one up. So can you hear me? Okay. So I hear what you're saying. I think it's more about identifying who you can physically get somewhere in a timely manner, and those patients should not get lytic, um, if you can do it. And so it's more about improving your system. I think that there is some data of really interesting data, Gershwick and Tony Gershwick had done it a couple of years ago, looking at the relative benefit of pharmaco-invasive to primary PCI as a function of your distance. So I think STREAM wasn't beneficial because these are going to be patients who are going to get primary PCI anyway. But when you're talking about a five, six, or eight-hour transfer time, then of course a pharmaco-invasive where you give the lytic and transfer. So I think you need to sort of identify your boundaries, but I I don't think that somebody who can make it within 120 minutes should be getting lytic.

Yeah, I agree, but it's really a point that a quarter of us have only given it. And so I always wonder if, you know, you can look it up and figure it out, but there was one instance, it was two years before I got to Colombia where they had to do it because there was such a bad snowstorm, nobody was able to get in, the FDR was closed, and they did it, and the patient did well. Normal coronaries, you know, when they got there, everything was solved. So I think the the key is whether, you know, we're going to be able to retrain people to to give it and give it appropriately and the correct dose, because an incorrect dose is obviously, and for sure, I always give the introductory lecture on reperfusion therapies in our hospital, and I always talk about lytics and warn them that it might be a boring topic because they'll never see it, but they need to know, they need to know the contraindications and the people who are at higher risk, etc.

All right, your turn. So you know, I think, uh, the trial setting is really helpful, but it is still a very, um, controlled environment, as we saw, right? So what we're not talking about here is ischemic time, there is transfer time, there is, uh, time to, you know, door in, door out, and uh, door to needle time and and door to sheath time, and all these things. But, um, ischemic time also plays a role. So I I think it does matter when did the chest pain begin, and how long did it take before they came into the hospital to begin with, and then take into account how quickly can they get to your lab. And unfortunately, we just live in an environment where practically, as as you've mentioned, every county is a little bit different. I mean, you know, there, yes, we think maybe that the ambulance can show up on time, and the next thing you know, half an hour later they're still not there to pick up the patient. I think we've all been in that situation where it's not always consistent. If you're lucky enough to be in a county where the transfer times are consistent, then then you can then you can count on that, but our transfer times are not always consistent across the board in the U.S. So I do think ischemic time takes into play. Maybe we can move on a little bit to the aspirin versus Plavix, uh, the study I'm joined with Prashant Khol and, um, as well as Rajiv Galati who just gave the talk, in terms of aspirin versus Plavix monotherapy. Have you guys switched over yet?

Uh, thanks Bonita, you fantastic summary, Rajiv. Um, yes, I have, uh, to a large extent switched to, uh, P2Y12 monotherapy, but I think the point that Rajiv made about, um, uh, you know, understanding periprocedural, perioperative issues and stopping that is is an important one. Uh, so you know, I'll switch back to aspirin during the periprocedural period. I mean, I don't think there's any data to do that, but it just makes it easier all around, and uh, that's at least what I've been doing. But, uh, I think that this is useful information.

Yeah, same. Venita switched to, um, clopidogrel whenever I have to use aspirin, but there are patients who also, most of the patients I don't know I see have afib also and concomitant anticoagulation, and in those patients I still kind of, if if there's been stable, then I just take both off and leave them on the anticoag, or just leave them on aspirin and the anticoag, just to reduce the bleeding. But otherwise, and you know, most of them I use Plavix. I like to, in our practice, I've got my head buried in the sand; I will do it sometimes, but I won't proactively go out and change someone who's been on a baby aspirin for a long time to say, you know what, the data suggests Plavix might be better, um, I guess that's just some personal bias. And I think these issues of discontinuing for orthopedic surgeries just makes me a little bit uncertain, and aspirin has just been around so hard, and the branding is so good, it's going to take me a while to really switch out. Well, some of my patients I'm going to follow long-term, the referring knows to call me, they're going to stay within the system, and it's, you know, I feel much more comfortable doing Plavix monotherapy because I know I'm going to get a call, I know the patient has access to the physicians in our network. And then I have another group of population who they get their PCI and they leave back to their home country or, you know, move out of state or don't have readily access to health care, and honestly, I've been less likely to do that in that population because I think the I think the outcomes after surgery off of no antiplatelet agents is is is is is scarier. We've seen some horrible event rates in patients who all antiplatelet therapy has been has been stopped. So I'm going to let Bonita introduce our next speaker, but I I'd say the one issue about the ass all this, uh, de-escalation and and single therapy, you know, that it's gotten so confusing for everybody, and and I think one of the things that groups can probably do is look at this data and think about it. I think there's an advantage if your interventional group does it the same way, and I don't know the right answer yet, and I think, um, that it's a great thing to have a conversation because maybe it's just we use Plavix as our standard, you know, the problem with prasugrel and ticagrelor, it gets expensive. So I but I think this is stimulating the discussion is an important thing.

All right, Bonita. All right, let's move on to thrombectomy, state of the art, if Dr. Anand Prasad can can come up. Okay. All right. So there wasn't that long ago where we were basically doing thrombectomy for almost every STEMI. I think many of you all remember that, uh, you know, the idea was why use all these drugs and things, why not get the clot out? And so we kind of did an about-face, but maybe we're re-looking at that concept. So some disclosures. So you know, why, uh, why do we worry about thrombectomy, and and what do we think about it? I think thrombus, particularly embolization during procedures, is really a big concern, uh, it's very frustrating, and uh, you know, when you have a thrombus that's there, if you can take it out, maybe that helps, but there's a lot of unanswered questions. So I'm going to go over the different aspiration catheters and different techniques we have for thrombectomy. A lot of this is a review.

For most of you, but maybe for the fellows, it's important to look at this. We'll start off with the simple manual aspiration catheter. These were the ones we were largely using, uh, five to ten years ago, and they come in a variety of different sizes, low profile to larger devices, many of which can be used in the peripheral circulation. The basic steps are shown here; essentially, you connect a syringe and create a vacuum, then you turn that stopcock and aspirate. It's pretty straightforward, pretty simple, and can be quite effective in many cases.

The fun part of Interventional Cardiology, you know, with thrombectomy was, and we still see it with some devices, you inject that syringe in that little basket; it's like, you know, panning for gold, and then you take pictures of it and show your family when you go home.

So here's a frustrating case that one of my partners had. It's a smoker, 45 years old. He came in late with an anterior wall STEMI. You can see the filling defect there and lack of flow. So essentially, TIMI zero flow. Heparin, glycoprotein IIb/IIIa inhibitor, angioplasty's attempted, and this is what you get after angioplasty. You see a big filling defect in thrombus, and then the distal vessels not filling. So you know what do you do here? Do you, uh, try to aspirate? Do you try to stent? You know, what can you do? So in this case, multiple runs of a Pronto catheter all the way down to that apex to try to aspirate, and this is the material that they got: copious amounts of vasodilators, all your microvascular dilators given, and you know, the patient's placed on an eptifibatide drip overnight. Low to adapt, brought back the next day for an angiogram, and it actually cleaned out the proximal part of that vessel really good, but you have a persistent filling defect. And unfortunately, in this case, they elected, you know, at this point down in the apical LAD, it's best to leave it alone, and you know, that they can show you how frustrating it can be to treat these lesions.

So, uh, we know it's effective at getting clot out, but why don't we do it more often? And this is a meta-analysis of the various trials that were done. Even though some of the softer endpoints, such as blush grade perfusion scores, those things look better, the hard endpoints really did not improve, and there was a concern of increased stroke with these procedures. And you know, you particularly want to be careful in the right coronary artery where you're manipulating thrombus and the ostium of the right coronary artery, and you're dragging it out; it has, uh, you know, not insignificant risk of going up to the brain. So just remember, as routine use, manual aspiration is a class III indication in our revascularization guidelines.

Uh, how many here remember Angiojet? So you know, we don't do a ton of Angiojet in our lab, but the principle was very interesting, right? You had these saline jets that are shot backwards and create sort of this suction vortex, uh, and, uh, theoretically, it's very effective at getting rid of thrombus. Uh, we remember the original Amy trial, which was a negative study; the big criticism was a lot of those patients in that trial had minimal to no thrombus, right? So it's hard to show a benefit. The Jetstream trial came sometime later, had more favorable outcomes with respect to major adverse cardiac events.

So, uh, pacemaker use is, is you know, something that's commonly done with really thrombectomy. Remember, for the fellows at least in the audience, as you destroy these red blood cells, you release the adenosine; you can get profound bradycardia, particularly in the right coronary. Blood loss, hemolysis are all issues, and you're still at risk of distal embolization. You know, it really kind of turns up and disrupts that thrombus.

The last Angiojet case we did in our cath lab in San Antonio was in 2019. This is an interesting patient. So you would expect this to be like an ACS presentation, but he came in electively as an outpatient for increasing angina. And I freeze the frame there that shows you that filling defect in the distal right coronary artery, and you can see it's like TIMI two flow down the vessel. OCT was performed, and by report, there was a lot of white thrombus, so organized distal white thrombus. A manual aspiration was performed, got some of the fragments of tissue, and, uh, post-aspiration, the flow you can see is better. Patient's placed on Heparin, started on DAPT, and then a few weeks later brought back, and you can see improved flow in the vessel but still a filling defect. So they elected this time to be a little more aggressive. This predated our use of Penumbra. The Angiojet thrombectomy was performed, and this is what the Angiojet on the left there looks like, and you see they started off without a pacemaker, right? So certainly they learned very quickly that you need a temporary pacemaker often with Angiojet use. And after Angiojet, the flow is better, but you still have that filling defect. And what I often tell my fellows is if you've tried a bunch of different things, there's still thrombus; sometimes just stent it, tack it up against the wall, and be done with it, particularly at 2 AM.

So in this case, the position is stent and deploy it and sort of treat that area. More recently, many of you now use the Penumbra system. This is the CAT RX, six French compatible, a 0.014 wire system, active suction, and the big question is can this active suction actually help prevent the stroke issue, right? So the important thing is to keep that suction going all the way through the guide and then clean everything out really well. There are some technical issues with Penumbra; you've got to be careful with it; it's hard sometimes with buddy wires, guideliners, things like that, but, uh, you know, it still can be a useful device.

Here's a case not too long ago. You can see the visible thrombus filling defects sitting in the proximal LAD. It's treated with several passes of Penumbra, and this is the material you can get out with the Penumbra, those little fragments of thrombus, and then after that, it's just a matter of stenting the lesion.

So, uh, what are the data for the Penumbra? There's a single-arm study, the CHEETAH study, which demonstrated a low rate of distal embolization and efficacy of the device, and that prompted the next study, which is an ongoing prospective randomized controlled study of the Penumbra system in ACS patients. So that's that's an ongoing study.

So in conclusions, I think routine manual aspiration should probably be avoided. The real management of thrombus involves not just devices but pharmacotherapy, some of which you've heard about, and then the Penumbra system's really promising, but we have to see if this can translate into really hard endpoint benefit in randomized controlled trials. Thank you. That was great. I, you know, the word routine is really important. So, um, you know, the clinical trials really took all comers, and and we shouldn't be doing routine thrombectomy. So this is sort of becoming now a niche device, which is harder to show benefit with in larger clinical trials just because you really do need to make sure you're enrolling those niche patients.

I do find, uh, in, in the particularly extremely large thrombus burden cases, specifically those that we saw during COVID, at least what we saw in New York, um, uh, I, we were using aspiration thrombectomy, particularly in a setting of intracoronary lytics. So this is once there's so much thrombus, nothing your usual routine is not working, and if you're considering giving intracoronary lytics, we would give it via, via an aspiration catheter just to maintain wire position, wait a few minutes or as long as you can wait, um, in the cath lab, and then do mechanical aspiration. Now that's all just anecdotal and based on our experience during COVID, but we did tend to use a bit more mechanical aspiration therapy during that setting because it was a large resistant thrombus. So I do think this is becoming a niche device. I'm going to go down the panel and see how often are, are you using aspiration thrombectomy? Do you have a particular, um, preference towards manual versus mechanical, and and what are the specific patients that you consider them in?

Yeah, completely echo your points. I think the word routine in the guidelines is important. I mean, I think there are roles for the aspiration devices. Personally, we use, uh, Penumbra, uh, quite often, probably more often than not, and then, you know, one of the other aspiration, sort of suction straws as I called them, which effectively is just what they are. And I think, you know, the art of medicine here kind of comes into play when you consider the size of the thrombus, uh, the likelihood of distal embolization of a larger thrombus that may push you towards using aspiration, and then of course, I think you have to also think about the adjunctive pharmacotherapy. So with large thrombus burdens, then I have a lower threshold for using a IIb/IIIa inhibitor as well.

Yeah, we are as well. The manual aspiration is so painful; you have to keep the negative suction; you have to be very careful about not injecting anything forward and things like that. But the Penumbra has worked really well, particularly in patients with large, large thrombus burdens. The patients that I can't keep their artery open after the first balloon dilation before stenting, kind of, sort of those are the patients that I think about using. And then, um, if the second balloon dilation doesn't work and it's all thrombus, then I use the Penumbra. So, you know, I mean, it's all being said, but I guess I'm cautiously optimistic about the future for device therapy in coronary thrombus. We're learning a lot from the neuroradiologists; they really understand thrombus properly, and I think we're seeing a lot of crossover technologies now. You know, Sentry, the type devices, proximal occlusion, all sorts of novel stuff that I, I won't be surprised if we, if that pendulum swings back again with a better device for routine thrombus aspirations, but right now, I totally agree, you know, stroke is a big deal; you've got to be really, really thoughtful before you pull a suction device out for a coronary artery. So I think, comma, then I'm going to hand it over to you to Tim. I think for the sake of time, we may want to go on to the next case, and I'll give you guys the next panel discussion.

Yeah, let's just ask a question, and we'll do the next. How many in here, of your, in your STEMI population, use uh, thrombectomy less than 25 percent? How many would say they use it more than 25 percent? All right, so that, it, I think it's probably we're following what it is, but I do think it's a challenging problem; they'll continue to evolve. So now we have four cases, and, uh, and then we have five minutes for the case and about 10 minutes to discuss. And so our first case, um, Constantinos, and I totally butchered that again. He's from Tampa, Florida, and, uh, he'll start the case. Thanks so much. That one's Manos is going to have to say it's very simple; Greek is everything, right? All right. So, uh, I'm, I'm going to present you an interesting case; I learned a lot from that. Uh, you want to put the presentation? Yes. Oh, okay. Seven. Well, while we're getting that talk loaded, I'll just make a final comment on thrombectomy. We've talked a little bit about technique, and I do think technique is really important, um, giving some vasodilators; I particularly like nitroprusside in that situation if the blood pressure will tolerate, since it will dilate the microvasculature in addition to the macrovasculature as well as being very meticulous with your aspiration movements. Uh, here we go. So no disclosure. So I will present about the case that was transferred to our institution from, uh, for surgery actually. So she was a 54-year-old lady, uh, non-STEMI; the story was he, uh, she got chest pains, she got dizzy, passed out. So it was not only chest pain, but it's also a syncope. I went to the other outside hospital; she was cast. She had three-vessel disease, and in addition, she had an anomalous RCA from the left cusp, but the city, anomalous course, the surgeons felt that it was too high risk, so it was transferred to a tertiary center for us for surgery. Two of the surgeons evaluated the patient, and they, they turned her down. Another surgeon decided to take care of the patient, actually refused after so many surgeons decided not to operate her, and they asked us to fix. I, I was not able to get the, the diagnostic from, uh, the initial one, but I'm going to show you the diagnostic from our cath lab. So anatomy was, it was a mid LAD CTO; there was a circumflex, 80 percent, and there was an RCA that had an anomalous course from the left cusp and a distal CTO. I'll show you the pictures. Uh, before we go there, I'll tell you that we had the CT that showed that the, that the RCA was coming from the left cusp, but also it had an anomalous course; it was going, uh, intramurally between the pulmonic artery and the aorta, and also something that we don't see very often in the CAT scan report; it said that it was a slit-like narrowing in the ostium that, by the way, we would not see it in the angiogram, with the 60-70 narrowing; it's very important for the decision of how to fix. So this is the RCA coming from the left cusp again. We didn't see the typical slit-like in the ostium. You could see the distal RCA that was CTO. This is the circumflex that had like an 80 percent simple type lesion, and here you can see the mid LAD that was CTO and filling via collaterals. So multiple lesion patient with a non-STEMI, ejection fraction 40-45 percent, chest pain free. So the question would be what we'll do next. So what do you fix? You fix the circumflex, you fix the CTO of the LAD, CTO of the distal RCA, or you fix the anomalous RCA? So I'm not sure if anybody wants to take the question. There's a lot of lesions, uh, patient turned down, uh, refused surgery; she refused. Oh, that is a very good question, because in my mind, this is an easy surgery, like it's just a bypass, but apparently, I discussed with the surgeons why would the surgeons refuse; apparently, the surgery is not, is more, uh, difficult than what we think, because they have to unroof the intramural RCA and may, that have to reposition the ostium. So I'm not sure; I don't think there's any surgeon here, but apparently the surgeons, so it was a very high risk surgically; it's not a simple, a simple attachment of the grafts. So again, we know that it's a risk of sudden death, and it's very important because the patient actually got chest pain and passed out. So what if it was an arrhythmic event? There is very little studies about PCI for anomalous coronaries; there is some data, but it's only case series; we don't have much information. So the question for us is, initially, we thought that the mechanism of why people are, are having angina and dying is because of, uh, of compression. We think that in the proximal segment there's a compression during exercise; the aorta and the pulmonic artery dilate, they compress the right coronary; this is why people have angina, but most recently we found out that this is not the case; most probably the mechanism is like the pulling of the RCA from the ostium, and actually there's a kinking of the RCA that becomes important about where to fix; do we put the stent in the proximal segment or do we put a stent in the ostium? So surgery would fix that; that's a class I, but, uh, for, for specifically for our case is what do we fix? This is one of the old publications that you can see the slit-like in the ostium of the RCA. So we know that if we're going to put a stent, we're going to put it in the ostium, and we want to protrude it in the aorta. So this is what we decided to do; of course, we start with the, with AZK, with easy coronary; that was a very easy intervention to the circumflex. I will put the 2.5 by 25 Zion balloon stent; post-dilation; good result. Then we went ahead, and we thought that the next most important intervention would be the CTO of the LAD. So again, it didn't take us, take us too much of a contour radiation, uh, so we were able to fix the LAD. So after this intervention, we had fixed the circumflex and the CTO of the LAD. Now the question was, we still had enough contrast and radiation to work; so the question was, do we fix the distal RCA CTO or do we fix the RCA anomalous? So the challenge was, uh, what do we do? Do we put one long stent from the ostium to the proximal, or do, if it's just the ostium or just the segment between the aorta and the pulmonic artery? So, and also depending regarding the stent, do you understand with a lot of radial force, so in case it's between the aorta and pulmonary artery to keep a radial force, or you need a stent that is very soft because with the slit-like stenosis, you don't want it to be too tight in the ostium. So there's a lot of questions. So what we decided to do, we went back; there was a publication with a series about using IVUS in order to determine if there is a lot of stenosis and the butamine challenge in the cath lab. So this is a publication that shows that in the proximal, in the, in the picture in the left, they did the butamine challenge in the lab; they put the IVUS, and they figure out what was the segments that would get more narrowed, both in the proximal RCA and in the ostium. So we pretty much tried to reproduce this paper. So we acquire the RCA, and we put, we put our IVUS in the proximal, and we give the butamine; we started, we went up to 20 micrograms per kilogram, and we pretty much start seeing; the upper pictures are actually in the, in the proximal RCA; it was very interesting because you could see; we could, we could advance the IVUS, and we see where the RCA was actually getting compressed, and we did the same thing in the second picture in the ostium. So in the ostium, you could see where the, the, the artery was getting compressed in the ostium, and that allowed us not only to see the size of the stent but also we were able to calculate the length of, because geographically you cannot tell, uh, what is the length that the artery passes between the pulmonic artery and the aorta. So by, by continuously giving the butamine, advancing the IVUS, we were able to calculate, uh, the length of the segment that was compressed both between the aorta and the pulmonic artery, but also in the ostium. So both, both mechanisms appear to be present in our case; so both there was both compression and was also pulling in the ostium. So what we did, based on it seemed to be like about 30 millimeters of narrowing, so we, we put the follow by 38, and again, some of my, we discussed a lot with the different attendings about, and a lot of them had strong opinions, actually one attending said that maybe we should put two layers of stent where the compression was between the aorta and the pulmonic artery just to keep a more radial strength, uh, and some others who say that we should put just only a short stent in the ostium so we don't risk a fracture, but finally, we decided to put one long stent and cover both the segment of compression and the ostium. So we put the 4 over 38. So after the end of the case, we decided to leave the distal CTO of the RCA alone. So the things I learned from that, from that case, it was very interesting to, to do is that actually there are two mechanisms of angina and sudden death in those patients; it's, uh, it's the compression and it's also the pulling of the coronary artery, and it was a fun technique to give the butamine and actually estimate where the, until what territory of the RCA there was a compression, and that is pretty much my case. All right, Constantinos. Thank you. That was, that is a great case. So my only comment, we have about five minutes. Yes. My comment is if he showed that case to 20 different interventional cardiologists, you'd get 14 different rationales and approaches. So there's so many things to talk about, but Jacqueline was looking for the microphone, so I'm going to let you start. [Music] Uh, that's a great case. I, I guess I have two comments; one is just more, um, obviously there's so much difficulty in discussing with a patient, and the patient probably had some, um…

Difficulty making a decision, but with the anomalous right end of the total LED, I don't think it's unreasonable to try to re-have that discussion with her about surgery. I'm not sure of the logistics of what exactly happened with the discussion, but I think this is somebody who, with a total lid and the anomalous right, is really what bothers me.

The second question has nothing to do with the case. The case was very interesting, and I love the points you made; it was really nice. The question I have is, um, the rationale for the use of the Impella. Um, and uh, I think that, just like Tim said, everybody would have a different approach, but what was the rationale for the Impella?

The rationale was that it was a three-vessel case, and to be honest, we're not sure of how much we would move forward. We did not know if there would be a complication, and we also anticipate, given the butamine, which could cause ischemia during the procedure, so we put—just to be for everybody to be comfortable during the case—again, if we had the complication in the LED, that would be the—we would have only the OM1 being open. You understand that there's a CTO of the right, CTO of the LED, so one complication this patient—that would—that would be catastrophic. So we decided to put the Impella for protection, so just to give us the time, and again, we thought maybe during the Butte I mean, Facebook start getting ischemic, get arrhythmias, we're just going to do the procedure without any issues, and those are major points.

So one of the things I've started doing, especially earlier, um, in my career, you know, you I sort of wanted that protection more, but you realize with the Impeller comes a lot of other issues, a lot of complications, still a 14 French device, and of course, the associated cost. And so what I've started doing that has really helped me avoid Impellas in a lot of cases, just to sort of share, is I now put a PA diastolic catheter for all my complex cases. CTOs not as much, but any of my sort of low EF cases, even in EF of 25 that I'm going to do a left main on, and if I have a good PA diastolic, I watch that PA diastolic throughout the case, through my balloon inflations, and I have an idea of whether or not I'm going to get into trouble based on what my PA diastolics are doing, and that then could help you decide to stage something like this as well and say, you know, okay, my payday stock is driving up, maybe I'll bring back for the anomalous or some of that, but just a thought. Very, very nice case, and then very nicely presented.

Yeah, thank you very much, and great case, and you know, this—you could spend an hour unpacking this case. I'm just going to make three quick points. The first point is, I saw the anatomy; I'm not sure I saw the ischemic lesions. So we do a lot of PET scans, so I'm not entirely sure because for people who do CTOs, not all CTOs maybe ischemic, so that's one point. I mean, not to disagree with what you did, just saying that, you know, we often tend to do CTOs that were non-STEMI. That's good, PET scans. Yeah, it was not an—it was a non-STEMI, so it's not—yeah. And so we might do MRI just to see what the non-STEMI came from. Yes, again, I'm not just disagreeing with the strategist—stylistic thing.

Um, the second thing is, you know, we don't treat—at least me personally, I don't treat—CAD just for improvement of EF because for chronically low EFS, it doesn't improve EF; it's only acutely. So if the—if that was the rationale for using, say, Impeller, 45 degrees may not—maybe not—we wouldn't—might not have done it. And the third point is more of a technical thing: for these types of RCAs, we have stented these, and we can get good results, and yes, there's patency. I like to use a simple wire technique, so that way you have a wire to show you exactly where the ostium is because I had one case where we missed the ostium entirely, and the patient came back with re-stenosis. It was extremely hard to get back in, and so I think either use something like ostial flash, but then maybe that's technically challenging also, but simple wire works really well for this situation. So this is going to lead to conversations at 10 o'clock tonight at the bar, but I want to know, Bonita, what would you—how would you have done that case?

Yeah, so um, I didn't get a sense of how sick she was, um, but if she—if this was—if the Impeller was only placed for—for the anatomy, I probably wouldn't have—I would have done what Mega described—Donna Reinhard cath—gotten a sense of filling pressures, cardiac index, pulse pressure, things like that, and probably wouldn't have used a support device. And then, um, a beautiful job fixing, um, the OM and LAD CTO. I think again, if the patient was not super sick and stable, I would have probably taken her off the table at that point and done some sort of functional testing to get a better understanding of what this RCA is doing, particularly in the setting of the fact that the RCA has a distal CTO and uh, and and and it's all—it's already well collateralized. So I'm not—I'm not sure—I don't know the answer to this, but the on the, you know, on the flip side, the question becomes, um, is there potential harm in now opening this up in the setting of the intramural course uh, and and and and getting flow from—from the RCA and to grade versus retrograde from—from the left coronary system? Again, I'm not sure what the answer is; I'm just bringing it up as a—as a thought for discussion. So I probably would have taken her off the table at that point and done some sort of functional testing and seen whether or not I wanted to proceed with the—with the RCA. Any other thoughts?

Yeah, I—I agree. I probably would not have used Impella. I would have done the LED and the Circ and then stopped and put the patient on a treadmill and then reassessed. Um, so that's the technical part of it, but just to kind of follow on from, um, what Jackie said about the—just going back to the option of surgery, you know, just a philosophical point, as a—as a community, as a profession, we find it very difficult to say no to cases. So if the surgeon has said no, there's almost some kind of compulsion that now, because the surgeon has said no, we're obligated to say yes, and I think we need to revisit that mindset because it doesn't always make sense. And so the idea that just because a surgeon has said no that the PCI is also an option, you know, it's all in how the case—or—is presented to the patient at the end of the day. And so this is just a—this is not a criticism, just a philosophical discussion. Again, we could have this discussion for the next two hours, but just to sort of re-re—sort of iterate this issue that just because a surgeon has said no doesn't obligate us to say yes. All right, thank you so much for sharing that case with us. We're going to move on to the next case. Dr. Kechi Idioma is here to present our second case.

Case presentation in the QMI and Scat. I have no disclosures. So we have a 35-year-old man who presents with chest pain. His history is pertinent for diabetes. He's on metformin, Glipizide, Glucotrol. On his vitals, his blood pressure is normotensive; his tachycardic and tachypnic, and his troponins are elevated and uptrended. So an EKG was obtained, and that's his baseline a few months ago, and you can see there in this EKG with his chest pain, there's ST elevation leads two, three, AVF, as well as V4 through V6. So he was diagnosed with an acute STEMI. Bedside echo was quickly obtained and showed an EF of 43 with global hypokinesis. He was given aspirin, metoprolol, and a bolus of Heparin, and the cath lab was activated as well. In the cath lab, his credential images are shown, and you can see, um, in the LED pointer, but um, you can see that it diffuse narrowing of the mid-LED, and it's towards the distal LEDs occluded over there, and this is RCA in the—on the far right—and very minimal lumina irregularities. And so he was looking at the images; we diagnosed him with a type 2 SCAD. Still having chest pain, blood pressure is normotensive, and it's tachycardic. So the question for you is, what do you do next? You send in for surgical revascularization? Do you do PCI the LED, or do you consider conservative medical management? Show of hands for PCI, and show of hands for conservative medical management. Okay, well, we decided to do PCI the LAD, given his ongoing chest pain. I mean, I don't—however, we try to wire the distal LED, and as you would know, sometimes this challenge is getting that wire into the true lumen of the distal—we just couldn't get that wire into the distal LED. And so at that point, after multiple attempts, we decided that, um, he was hemodynamically stable, and we could treat his chest pain with nitrates. And so we decided to convert from a PCI strategy to a conservative medical management strategy. He was given nitrates for about 24 hours; the chest pain resolved. A CTA abdomen and pelvis obtained and that showed ectasia of the renal arteries as well as subtle beating of the renal arteries bilaterally as well as iliac artery ectasia. Um, a few days after being watched in the hospital for about three—three days, he was discharged chest pain-free and followed up in the outpatient clinic and doing well. His meds on discharge, he was on aspirin, metoprolol succinate, spironolactone, valsartan, and insulin for his diabetes. He would not put on a statin because his LDL was 55.

So on the key learning points for us were—it's important for us—is to recognize the angiographic features of SCAD, and we'll talk about those in a few seconds. For management strategies, if the patient is stable and there's no evidence of high-risk features, conservative management is the preferred strategy. Um, if for revascularization, if the patient has left main or severe proximal two-vessel and dissections, you may consider doing CABG. So the angiographic classifications of SCAD, real quickly, um, type 1 SCAD, um, there's—if you look at the angiogram, you see multiple radiolucencies. Type 2, there's evidence of diffuse narrowing, like just as in our patient. Type 2 SCAD is further classified as type 2A and type 2B, and type 2A, you have the diffuse narrowing, but in the proximal and distal to that narrowing, the vessel is normal, whereas in type 2B SCAD—SCAD, the diffuse narrowing extends all the way to the distal vessel. And in type 3 SCAD, sometimes mimics—it can be confused with atherosclerotic disease because there is just this tubular or just a short focal, um, narrowing of stenosis, and imaging can be helpful to distinguish between atherosclerosis versus type 3 SCAD. So for revascularization, when can you revascularize? For patients who have SCAD, if there's left main dissection, you want to consider revascularization. If a patient has ongoing ischemia, whether on EKG or clinically, just like in our patient, you want to consider revascularization. If the patient has TIMI 0-1 flow in a proximal vessel, you want to consider that as well. If they're unstable, cardiogenic shock, or if they have evidence of refractory ventricular arrhythmias, you also want to consider revascularization. Management algorithm: if, once again, if the patient is stable and there's no evidence of high-risk anatomy, consider—consider—consider—consider conservative therapy is recommended, and you watch them in the hospital for three to five days. If they are stable and have—but have left main or severe proximal two-vessel dissection, you want to consider CABG. If they have ongoing ischemia or any of the other things we talked about as high-risk features, you want to consider PCI if feasible or send them for urgent CABG. Here's an algorithm regarding PCI for SCAD. Important things, I mean, the different strategies, but if you're going to use a stent, it's important to make sure your stent extends about five millimeters proximal and five millimeters distal to the dissection flap. Cutting balloons can be useful in patients who have type 2 SCAD. Those are my references, and I acknowledge my preceptors at NGHM Mayo. Thank you so much.

Thank you. Great case, and it's nice to see that recognition of SCAD early on, despite it being a type 2 version, which often looks like coronary artery disease and sometimes hard to—hard to differentiate. Um, you know, for—for us, uh, we, you know, we routinely try to conservatively manage these patients as much as possible, but as you said, if the patient's having chest pain, it's hard to ignore that, and you do at that point sort of feel, um, uh, potentially compelled to—to attempt some sort of revascularization, and that would depend on—on your institution. I don't think I could get my surgeons to come in to take that patient quickly just—just, um, uh, for—for chest pain alone, and it was rather distal as well. So—so potentially attempting with a wire approach is—is reasonable if—if the patient is—is still having a lot of chest pain and ischemic changes. Um, of course, if you do get the wire down before you do anything, you know, in terms of stenting, which is not always needed in these cases, but if you do consider it, always use intravascular imaging because you may not be in the true lumen. So—so that's really important. And then the—the last comment I have before I move on to my panelists' comments on how they would handle those cases, um, you had mentioned left main dissections. I caution everyone, um, to remember that your guide can cause the left main dissection as well, and that's not all SCAD, no matter how much you may want it to be, and you should treat those with—with—with the—with the stent.

I didn't have anything to add in addition to that. I'm going to give up my time to the right honorable Dr. Galati, who's an expert on SCAD.

Yeah, I'll just add two quick comments. One is the meds after uh, SCAD; there's no real data to support use of statins and a second antiplatelet agent unless you stent, and maybe beta-block would be helpful in this situation. And the second thing is, if you stent, you can actually extend the dissection, so you really have to be careful about who to stent in these patients, um, and then these guys can have references right, so it's really important—the long observation as opposed to other ACS cases where you send them home the next day—you have to have that three-to-five-day period.

Thanks, Cassie. First of all, congratulations, you're no longer a fellow, right? Your first slide said fellow, so congratulations on your new staff position—or super duper—and evangelist, and I'm looking forward to Tim's comments here as well. So the start of the case got me intrigued: a 35-year-old male with diabetes. So when—when you see that and you see an angiogram and you're calling SCAD to me, I questioned the diagnosis multiple—multiple times, and I got to say I am not overly completely 100 percent convinced this was SCAD, and maybe it was. I think a perfect opportunity for intravascular imaging, alternatively a repeat angiogram in six to eight weeks to see if there's healing. Certainly an unusual appearance. Interesting to hear what Tim says as regards to—let's just say it was the pain comment. Remember, SCAD can be painful because of the vessel wall. Carotid dissection is painful not because of brain ischemia; aortic dissection is painful not because of aortic ischemia. So vessel wall pain—be—be a little bit cautious of using that as your only trigger for intervention, but great case, beautifully presented, somewhat uncertain—at least in my mind—on the diagnosis. Tim has a good amount of experience too, so I love that case.

And I love that case, and I have—I will say three things. So number one, uh, it's hard on an angiogram to see from here, and I think that recognition of SCAD is when it is the first challenge, and I think one is having a high awareness of who it might be, and I think Rajiv's points about being a 35-year-old with diabetic—it's not your typical—but it 75 percent of occurs in women, but it definitely occurs in men. And so I think without seeing the angiogram really close, it would—it is difficult to see, but so that's number—point number one: have a high awareness in young people without risk factors in particular. Number two: be aware when you look at the angiogram. Number three: this is SCAD STEMI. SCAD STEMI is different than SCAD non-STEMI, and I think that we had a nice paper in JACC a few years ago that I think shows clearly with—with STEMI with patients who have ongoing symptoms, ongoing or hemodynamic changes. So first of all, high percentage patients had left main and had cardiogenic shock, and with appropriate PCI, you can have excellent results, and in fact, the long-term outcome in the SCAD STEMI patients was better than the atherosclerotic STEMI, even though they are higher risk, more cardiogenic shock, more left main. So this case, for me personally, I would—you know, it's ongoing symptoms, the LED's closed, so I would have done PCI. I think it's very distal. I think CABG is really not a realistic option there. I think it's hard for me to not try to open that when someone's having ongoing symptoms of hemodynamic—but I agree with you, it's hard from that angiogram from here to see, but trusting that it is SCAD, I would have definitely tried PCI.

Tim, I was going to make a point that—so I was always taught—in my understanding is that the pain alone is just like the pain of a dissection—it will hurt. And so the idea is to look for ischemia. So if you have ST elevation, if you have arrhythmias, if you have heart failure, absolutely—or patients who are hypertensive, maybe have some ST depression and who haven't really made enzymes—I think you can make an attempt at, um, at a conservative management, and then if they start infarcting or showing signs of instability, then you bring them in. And the other two points I'm going to make is that cutting balloons do work for this, uh, and and you don't have to always stent after that. And the problem in stenting is that the hematoma will often leapfrog the stent and go downstream, so that's—we—rather than the hardware is stenting doesn't necessarily work; you have to post-dilate, what not. So try cutting balloons first if you have to do it. There's a comment in the back.

Yeah, I just want to reinforce what you just said. Um, I think PCI has failed often in—in SCAD because PCI—uh, because it's a wrong way of doing PCI is—if it's a poor understanding of the pathophysiology of a hematoma in the wall that needs to be released, and if—you know, I've—I've—must have done about five or six cases since we published that case—little case theory, but we've done a few cases where we did star—so we basically used a small—small wire—and—and once we've secured wire into the true lumen, we parallel wire with it, and we—we opened up the vessel and restored TIMI 3 flow, and on the OCT, we could see very nicely that the compressed false lumen as has been evacuated. So I think in the future—and I don't—I don't—I don't advocate—I think conservative treatment has been—has been—and will remain—uh, the cornerstone of treatment of SCAD, but in cases where you have a STEMI and you're completely occluded, you have to do something, and cutting balloon is—is feasible, but you got to have a wire down, and the problem is that failing to wire a SCAD is because you're wiring the dissection, and at this point, you gotta be able to solve this issue and getting down into this vessel and therefore going and adopting some techniques that apply to CTO PCI and starring the vessel can restore the TIMI 3 flow.

Tim, can I make one more comment?

Tim, so the nice thing about being the moderator is you get to make the last comment before we go on. So—so I—I—another—I think a key point about this is whether you have a type 1 or type 2 or type 3 dissection. And then type 1 where you actually have—of—you are a dissection. Type 2 is more of an intramural hematoma, and so I think there is a role for cutting balloon.

Tim, can I make one comment? Uh, just because it's got a big audience here, and I want to make a couple of points, right? I've seen three thousand SCAD angiograms, and I just want to tell people not to think the cutting balloon is the answer here. I think fenestration stent is a fantastic answer. True SCAD vessels will—will fenestrate if you stent.

At them. They're so fragile. You just need a balloon, a one-to-one balloon at two, four, six atmospheres. I would be very cautious about shoving a bladed balloon than a young woman's super tortuous artery. To fenestrate a balloon angioplasty alone is all you need. My second carbon actually to agree with you, Tim. We have swung too far from conservative management and scarred a two, uh, too far to the conservative direction. I think there's an opportunity to reevaluate and lower our threshold to intervene, but I would use a balloon angioplasty, non-cutting balloon approach. But another great case, and now we're going to go on, so Dr. Doshi gets to talk about my worst case of the year.

Who gave you this talk, Tim? I thought it was you, just because you were trying to get back at me for something. I'm not sure, but with that being said, this case comes in two parts. It's uh, misery that happens twice, and I'll walk you through what transpired. So, um, I apologize. So this is an 89-year-old pathologist. So, um, obviously this is a person that is actually very well revered at our institution that had a history of coronary artery disease, status post PCI with atherectomy several years ago. Has the history of afib on anticoagulation and has a history of wall-controlled myelodysplastic syndrome. And he presented to a sister institution with neck pain and shoulder pain, not typical chest pain, but an EKG was done that showed potential ST elevations, and I'll show you what they look like. And then subsequently thereafter, without any sort of intervention, it resolved on its own, but a troponin was sent that was markedly elevated. And so under when a diagnostic cath that showed calcific RCA disease and was transferred to our Institution for our high-risk PCI.

So here you can see that the inferior leads have some degree of elevation, and then subsequently it resolves. There's still T-wave inversions in the lateral leads. And so this is the diagnostic cath that's performed at our sister institution, and what you can see is obviously there's a great deal of calcification even before any contrast goes in, but you can see calcium on both sides of the artery, kind of showing you how calcified it is, and there's a calcific nodule in particular, which is probably the mechanism of his ACS. So the question is, you see this, what's the next plan, and what do we do? And um, I don't know if you want to pause and maybe talk to the panel, or I can tell you what we did.

Sure, we can talk a little bit about um, um, what next, but I I think something that you brought up was really important, talking about the nodules. And when you see this degree of calcium that is probably riddled with nodules, and you don't need um, if you were able to get an intravascular imaging catheter down there, I'm sure that would be see that, and that's a mechanism of acute flat Proctor eruptive nodules can can can cause plaque rupture. So um, I'm thinking a supportive guide, a supportive wire, and anything that will allow me to deliver equipment easier.

Yeah, so exactly right. I mean, the three mechanisms of ACS are plaque rupture, erosion, or a eruptive nodule. And so the thought here was obviously this is going to be somewhere tortuous, it's going to need some calcium modification likely given the degree of calcium. This is probably going to be an atherectomy case up front. So can I make one really quick, and I I guess I'm biased by this is my worst case of the year, but I think we should go back to Dr. Call's comment earlier, you know, that I think the point is this is an aborted infarct. You have a little time to have a conversation with the patient and think about what you need to do. And now that it's aborted, having adequate medical therapy and being very thoughtful because there is a lot of potential danger right there, and so I think um, not having to rush into it is an important thought right here.

Absolutely, Tim. So uh, when he was transferred over, he his pain was improving. It remained on some level of nitro that we were slowly able to wean off. So there was a risk-benefit conversation that we had with them, um, so it was not done on the same day or even the next day, actually. It actually took a couple of days, um, so for him, we knew that this was going to be an atherectomy first strategy. He's 89 years old, and in patients that are really elderly, again in my experience, there have been times that despite using ammonopholin or things like that, they still have some degree of hemodynamic stability with atherectomy. So we put in a temp wire, frequently don't put in a temp wire, but in this case we did, and so for French temp wire was placed in. We went with a femoral approach, we used a long sheath, and they subsequently used a very supportive guide, a seven French AL 0.75 guide with a guide extender. Looking at the actual guide here, probably not providing as much support as we would like. Maybe I would have gone with something else, and you'll see why that'll be important in a few minutes.

So initially we could not cross this calcified nodule with any sort of Workhorse wires. So we backed it up with a microcatheter, used a polymer jacketed wire, a Xi'an black, and then subsequently were able to wire through distally, follow that with a microcatheter to swap for our atherectomy wire, and we used. So typically I use a caraval microcatheter as my first catheter because it has the lowest profile, but it has the least body and least push ability. So then when that wouldn't go, we moved to a more supportive torquable catheter, which was the turnpike spiral, got that swapped out for the Viper wire, and my plan was to do atherectomy with um, with orbital.

Now, quick question for you guys here: do you have any concerns for orbital versus rotational? I I personally I think it's dealer's choice here. I mean, I think you could make a case for either, um, the Glide assist feature with the orbital may help you around the bend depending on how far your guide extension is going in initially, but um, you know, I think I think either would work. I I wouldn't have any concerns with orbital.

Yeah, I felt the same way, and so we went with orbital for this one. Now uh, we have the Viper wire placed. We did six passes at 80k. So I went on the low speed, there's low speed and high speed, high speed being 120k. Most of the complications in the clinical trials have been at the high speed portion, not at the low speed portion. So we, here you see that we basically have to rectumize down into the vertical portion, subsequently go past the actual nodule, and then we go back and forth. And again, unfortunately I don't think it actually shows here, but then when we took our Crown out, what we noticed is that there's something right here, and again I don't think unfortunately it projects as well here, but there's a piece here, and what the piece is is that the crown has separated from the drive shaft. So we were able to get the drive shaft and everything out, but there's a crown that's here that's now uh in this calcium. So may, again, just maybe to pause, maybe I'll ask the panel, when you see something like this, what would be your next move?

And down alongside of it and perhaps inflate that to to drag that backwards, um, there's a couple of steps, especially since your wire is still in place, um, uh, that would probably be my first move before moving on to trying other techniques like twirling the wires and such. I think it depends on how much is in there. I think your best option would be just to stent over it and exclude it because it's kind of in a location where it's difficult to snare. Do you have any idea if it was just the actual crown itself or there was some part of the shaft attached to it?

Unclear, but um, I would assume it would be Crown in some shaft, um, we I know the answer because you're going to see what happens in a few. You had the rest, you had pulled out the rest of the device. The rest of the device came out. Yeah, it's just this portion which was the proximal portion. It's kind of interesting, just about four hours ago I was having a discussion with CSI about this exact issue, and it's very rare to see this in the absence of very severe tortuosity. I mean, there's some tortuos to you, but not enough that you would expect this would have happened. So why this happens, actually a different discussion, which is also interesting. You have a guide extension, and I would take that guide extension down alongside it or close to it, um, this this piece is still on the wire, so if you're able to take the guide extension down to kind of uh envelope this piece, and then you take a blue next to it, you can trap this piece within the guide extension, hopefully pull both back.

Yeah, so a couple of things that we did. One, I wanted to make sure that we had access to the distal vessel. My plan was to pull the wire back with the actual crown on it because of the way the construct of the wire is, but I wanted to make sure that I had distal access, so if there was dissections, which I presume there probably were, that I would still be able to do my PCI. And so I tried multiple different uh ways of trying to wire distally, you know, multiple different wires from polymer jacketed wires with increasing tip loads, but was unsuccessful. Use dual Lumen microcatheters to try to be able to deliver a wirelessly, still learning successful. But the thing about the Viper wire, which is very similar to the rotofloppy, is that essentially it's a tapered wire, but then actually has an O114, and so it goes from O112 to O114, so the crown can't come off of this usually as long as the wire is intact. So as long as you pull the wire with the crown in block, you can take everything out. And so essentially were you able to get the guide extension down further since it's just the crown and not the shaft? Because then perhaps you could have put a second wire. The problem was not through the god extension, the problem was where the actual um crown was. I couldn't get a wire around it, so it would either go sub-intable or would not pass it, and so that became the issue. But either way, so what we did was basically did exactly what Prashant said where we moved removed the Burr and Viper wire and block, took everything out, and then I tried to re-attempt to wire this, but either one we kept getting sub-emptible in two areas, one proximally and one around the area of the actual nodule. And then I looked to see retro options because I was like, okay, maybe I'll just go retro through the LED septals and then take care of it that way, but really the only retro options that were visible, I mean we could blindly serve septals would be it was to an RV marginal that was fairly proximal. So at that time he had no chest pain, was hemodynamically stable, and so the thought was let's just let this area heal, we'll come back to fight another day. And so this was misery one.

So what ends up happening is this is a crown, which you can see, this is what we were able to remove from the body initially, and this was what was left behind, and then we were able to get that portion out. So the patient did okay, uh, had inferior hypokinesis, LVF remained normal, no Frank chest pain, but now started to have exertion shortness of breath with exertion, which he didn't previously have. Also had bouts of NSVT that he, the longest being 10 beats, and again didn't have an SVT before. So the question here is, you know, do I try to reattempt this or do I let this heal and then bring this patient back? Ultimately, with talking to the team and the rest of our colleagues, the thought was why don't we just go ahead and read and just do repeat angiography? You'll see what happens. I think the outcome might have still been the same, but what we ended up doing was going back, but this time because of the fact that we had gone with uh, with Rota with orbital, and we actually snapped off the the distal part, we said this time we're going to go with rotational instead because this area still needs to be taken care of.

So again, same guide, same temp wire, and then took a little bit of work and were able to wire it with a polymer jacketed wire. Took a little bit of work just to get around the proximal dissection and then the distal dissection, but that healed enough that wiring integrate was much more straightforward. The problem was that when we tried to swap out for for our rotational atherectomy wire, the road of floppy, the microcatheter really wouldn't pass. So we basically had to bury the microcatheter and then free wire with a rotofloppy, which is what was the road to drive, which is what was done. So uh, the plan was to do rotational atherectomy. Started off with a one Fiber. One fiber really wouldn't pass around this bend, so then we downsized to a one two five Burr, got uh multiple passes, and then upsized to a 175 bar. Again, this is all through a seven French, so both of these could be accommodated through a seven French. During the one five bird, there was Mile St elevations, and then um, and then afterwards they were about the same, and they were sort of subtle. And so the thought was maybe, you know, we had dissections previously, maybe, you know, they got a little bit worse. So the plan was to very quickly modify the plaque and then lay as much metal as quickly as possible over supportive wires. So we actually switched out to a grand slam two long stents, replaced, optimized, but the problem was right after that there was a full minute no Reflow. And so when this happens, essentially the thought was, you know, is there a stent edge issue or it does it just it was it from our atherectomy given how much calcium there was, the patient was elderly. So if I'm going to Reflow, we ended up, you know, again confirming with IVUS that there was no thrombus, no standage issues, and a ton of vasodilators were given. So nearly a microgram of nicardipine, I gave around 350 mics of Epi, I even gave nearly 500 micrograms of uh, sorry, I have 500 micrograms of adenosine, and despite all that could not restore flow for the life of me. We also put a dual Lumen microcatheter distally and injected just to make sure that there was some outflow to see if, you know, again there was something technically that needed to be optimized, but the answer was no. So this patient went into severe had developed severe chest pain, respiratory distress, was intubated, and again we really couldn't restore flow despite everything we did. So ultimately a balloon pump was placed, the patient was started on levofed supported and had persistent ST elevations, and the thought was now where you just have to unfortunately ride this patient out because there's nothing we can do do for the distal vasculature that we've plugged up with our atherectomy. He had a long clinical course, but just to get to brass tacks, ultimately he did not do well, was discharged with home hospice, and unfortunately passed away. So a very tough case.

So a couple of questions: one, you know, the initial Rota versus orbital apparectomy decision for the first case, I don't think it made a difference, um, I think unfortunately maybe if I had to use Rhoda, the uh the orbital might not have gotten stuck, um, were there certain things that could have done to reduce Burr fracture? Again, I used the standard technique of going one millimeter a second, listening for any sort of D cells or anything like that, and really didn't have any. The other part is in the second case, because we had proximal dissections, I didn't inject as much as I should after our atherectomy runs, and that may have delayed our recognition of slow fluorine or Reflow. And then the other part which has now changed my practice is I now routinely give vasodilators prior to any authorectomy run to try to minimize the chance of something like this happening. So I'll stop there and maybe open it up to the panel.

Wow, great case to show. Thank you so much for sharing that case. These are tough ones, and I think we've all been in this position of horrible, horrible uh, no Reflow, no matter what you do. You're looking for an edge dissection, hoping for an easy fix, you're looking for some thrombus that you can aspirate out, and it just doesn't work. I do think putting in a balloon pump at the end was a good idea because I do think sometimes a bit of that augmented flow and diastole can help in in patients where you've tried everything else and and nothing else is um is restoring flow here. I agree with your comments in the sense that you couldn't have predicted this Crown fracture. I don't I don't see how anyone could have predicted that.

Yeah, I mean, like, and even even if we had used potentially atherectomy the first time, um, you know, you still would have had potentially no reflu or slow flow. So again, the only thing I think I could have done differently is use a lot more upfront vasodilation. And so again, this case is sort of alter my practice as a result. So, you know, it's unclear to me exactly why he had no Reflow, could have been that threatened me, but it also couldn't be from the stenting. I think there is, we've had patients where came in with the non-STEMI, you put a stent in, you optimize it, and the post-dilitation will then cause in these elderly patients it's no Reflow that just persists, and we had a patient a few months ago, we ended up on ECMO because nothing would work, and he did make it out, but he was again in his 80s, um, and so one point I was going to make is, you know, what we may have done is perhaps use an impeller, just because I think there's some evidence that reducing um unloading the LV might have actually helped with the myocardial resistance and improved flow, perhaps. I don't know, I mean, uh, I don't use a whole lot of impel necessarily, but but this is one situation where we may have considered it. The kitchen sink approach. If you had just a really quick, first of all, lots of excellent technical skill that you showed on there, but the potential hazards of that case are going to start for terrible backup to start with, and number two, the combination of severe calcium and thrombus is a bad combination. And um, so you know, you could go on this another case, we could talk about this for an hour, the different aspects of it, um, and I think again this is where you know being an Interventional cardiologist can be a very humbling profession, right? And I think this is where you uh, you have an 89-year-old intelligent person that you have that discussion at the beginning and make sure that they know what you're about to do or what you're about not to do, is it is a really complicated. I think that initial decision, do you do anything or not, was probably the most difficult.

All right, thank you, Tim. I think the um, just to go back to this issue of the bow fracture, I mean, it's a just to be clear, it's a very rare event, but if you look at uh the times when it has happened, when when the company has looked at the times when this has happened, it's almost exclusively in the setting of significant tortuosity. And so the fact that there wasn't that much to atrocity here is kind of very interesting to me. I mean, the only thing I can imagine is maybe the the crown got stuck on a nodule or something, and you know, that that's the sort of cause here. So I don't know what to say about that, um, and then with the no Reflow of this sort of Second Time Around, um, you know, I think just longer pauses between runs is also another way to sort of try and prevent no Reflow, but you know, it's a difficult case. Sorry. Thank you so much. Thank you so much. Our last case will be presented by Dr. Michael Megley, who has um the easier task of presenting uh his best case of the year.

Well, yeah, it's uh it's much easier, so I'm actually going to change the mood a little bit and uh because I chose this case now because it's the best technical case or anything, it's just the best confirmation bias case that I had this year, and I uh that's what I want to talk about. So the half ref dilemma, and I know why are you saying this in uh in an ACS presentation, but I'm gonna share with you first of all the New England Journal of Medicine revive trials had among patients with severe left ventricular stocks function uh we didn't

Find any value of PCI in terms of death or, uh, reconnaissance, re-hospitalization? We all have these anecdotes, uh, maybe we cannot just talk about them very well. We all know that improving EF is here with better outcomes as well. So, and I think I heard that comment just before I came here, that PCI and several VEF, yeah, does not do anything. So I know, I know that this is an ACS presentation and the trial we’re only on stable patients, but you know, please bear with me.

The patient is a 68-year-old gentleman; he’s actually a retired physician, so he knows better for himself. History CKD4, planned to have dialysis. He has known HFrEF for three years, yeah, for 30—for three years, following up with this cardiologist. He had a normal stress test, never had a diagnostic angiogram. Aggressive medical therapy, and we saw him; he was in three Asians guideline direct medical therapy was a beta blocker, interest though, and SGLT2 inhibitors. He actually had ICD in place, so he cannot be more optimized than this from a medical standpoint. He had recurrent admissions, heart failure in our hospital, another hospital, anyway. He came to this hospital this time with some chest pain on top of his HFrEF decompensation. Tripoli went up to six, I mean, in the setting of CKD4, fine, but still went up to six. We repeated Echo; it still shows the EF 30, not much different from prior Echoes, so nothing much different this time to go and did a diagnostic angiogram. RCA was fine; I was really conservant, die, so I took just a few pictures. Here you see on the second image; this will work, yeah, I think so. So there’s kind of a calcified nodule here, not very clear, and you know, Austin, the circle is not very clear on this AP column; it was more obvious on Ibis, but uh, we had this. I pulled it out and I talked to him; of course, he’s a retired physician. Heart team approach, and I really, I really thought that this was significant; not everybody believed it, but we’ll prove it in a bit. Uh, talked with him; he totally understood; he didn’t want to do surgery by any means, and he understood he will be, uh, going on the ELSA’s anyway, either way you go to surgery or PCI. Our team approach is not convinced; this left me and said, you know, IFR before we do anything, so I will take him and let’s say we’re gonna do this left main.

My first decision was, well, am I going to use MCS or no? There’s a lot of algorithm; I’d like to check at least three boxes, and if I get the fourth, it’s great. So he had a left main unclear involvement to the Circuit; will need atherectomy; his CKD4; he will have pulmonary, you may if something wrong goes—wrong, and his EF was 30 percent. So all this made me lean towards Impella, but I still did the right heart cath. I did IFR first; left main to LAD was 0.61, so it was clearly positive. Right heart cath showed an wedge of 18, cardiac index 1.7, so I said, fine, this is my first check mark; I’m gonna use Impella. So I put an Impella. Um, this small branch, I tried to get multiple wires, angled micro Catherine, and couldn’t do it. The only thing that I didn’t try is, uh, reverse wiring; was about to use it, but I kind of used a little bit of contrast already, so I knew that I had a bigger fish to fry, especially I started to have some pain, so I just tented across it and I wanted to move forward with the left main. So this was the left main on another projection; it’s clearly positive now, you know, and this again is kind of a calcified nodule, and I had a lot of options; IVF rotation, atherectomy, rotor shock, or orbital atherectomy. I don’t think it matters, but does anyone have any preferences this kind of lesion?

Foreign. No, I did not image before; I knew that it would not cross, and I know I’d use atherectomy anyway. I am a jafter, you know, in, in most situations they work equally well; I think just the one advantage is sometimes, uh, the Burr has more of a nose cone, so it’s a front cutter, and CSI isn’t. So there are some cases rarely where the nose cone, the sort of the, the tip of the CSM may keep it from actually, uh, touching it, but more often than not the both of them work well. Yeah, I, I this case specifically I didn’t think that I’ll have I really need front cutting, so I kind of chose to use orbital atherectomy. The only problem with orbital atherectomy in uses the nodule; you have to be, you know, cognizant of the Snowman effect, which might cause perforation; this when you have a small vessel, you keep shoving the tip of the nodule and you keep rotating into the healthy vessel, uh, the only way to identify is OCT, then have OCT, but I was very careful what I do, and I, I thought the left main was big enough to tolerate it. I did multiple passes at 80k, just one pass at 120k; I got away with it, and uh, end up with IVUS guide the stent thing, and then I crossed into the Circ; it was severely pinched, and I could see with Ibis that needed, uh, to be done, so I, I found the angle very, very, uh, friendly to do tabs, so I did Tab, and then afterwards I didn’t really want to lose that big Circ; I get another tap anyway. The case was very straightforward; finished with 100 cc of contrast, a little bit higher than I wanted, but I think a lot of contrast was, was spent on that small branch that I couldn’t get it the first time. Anyway, a patient was weaned off Impella, closing Manta; stayed in the hospital five days, Craig and worse than he needed, uh, dialysis. The only medicines I added are aspirin and Amlodipine; I didn’t add any medicine for HFrEF, so he was on the same medicines that he was on with her face with heart failure, EF 30, three years, but three months later his EF improved to 45 percent. He stayed outside the hospital, and then for still nine months I saw him; he was still outside the hospital; didn’t come back; I still, I think I repeat another Echo, but, uh, the best thing about this anecdote is, uh, you know, he was already on maximum medical therapy; I didn’t advance it much; there was no difference here; all what I added is PCI.

So what I kind of learned from this case, you know, MCS, uh, right heart cath is a must, although I had three checkpoints, but I right heart cath helped me to confirm that I need to use Impella here. A really important lesson I learned from a case before that that made me stop at the right moment is not to get stuck on a small task; focus on the big picture, and I had a lot to do up there; I didn’t need to keep chasing the small branch. Again, orbital attraction, centric nodules; it works pretty well; I just have to be careful and using a bigger, big enough vessel, and again, circumstantial evidence; it’s not an evidence; it’s just an anecdote, but I think it’s a, a pretty good anecdote. Thank you. Thank you for that, and I’m going to pass it over to Tim in a moment. I just want to make one comment for the orbital atherectomy and eccentric nodules; you know, I, I think it’s fine; it could be potentially, um, considered preferred if the Lumen was slightly larger. I think when the Luminous is as diseased and sonos as it is, it doesn’t really matter; the Rotibur will make contact just as well, um, so that was, that was my, yeah, all right. So anyway, this is a great session, um, I’ll end with that one, Mike, with just one comment for us says I started my career at Hennepin County Medical Center, which has probably one of the largest dialysis, uh, populations in the country, and, uh, I think one thing for Interventional cardiologists to really be thoughtful about is this is really one patient population where PCI is not better, and I will tell you I would have had a long, long, long, long conversation, as long as you know that the left main is normal, I would have a long, long, long, long conversation that CABG is a better choice for you, and that’s a great result, and I’m happy that got better, but I think in a dialysis or soon to be dialysis patient the data really looks better for surgery than it does for that, and that was a nice target for CABG. I agree; I mean, he’s a retired physician and he absolutely didn’t want it anyway. Thanks everybody; that was great, and so talk about one more announcement.