Dr. Marc Sintek, MD provides an overview of PCI, how we do it, and why that matters. Dr. Sintek will also share some case examples and some of the complex PCI tools used.
Doctor Mark Sag um who earned his medical degree at the University of Nebraska College of Medicine in Omaha, Nebraska. He then completed his residency in internal medicine uh at Barnes Jewish Hospital in Saint Louis. He stayed at BJH to complete his fellowships and cardiology, interventional cardiology and structural interventional cardiology at Washington University School of Medicine. He is currently an assistant professor of medicine in the cardiovascular division at Barnes Jewish Hospital. And his research interests are aortic stenosis, complex coronary interventions, coronary physiology, intravascular ultrasound cardiovascular disease in patients with rheumatoid arthritis. So thank you so much, Doctor Sytek for your time today. We really appreciate it and I will let you have the floor. Ok, perfect. Thanks for the introduction. II. I usually don't like people introducing me because it's just weird. So that's too much stuff for you because I did it for everyone else. So that's OK. That's fine. I mean it sounds like the previous topic was quite a bit different than this topic. So that's, that's also good. Keep people on their toes. Um Can you guys see my slides? Ok. Um And things like that? Yes. The, the life. Ok, perfect. Um, and so, um, please, you know, feel free to interrupt, um, put stuff in the chat and things like that. Um, it's a pleasure to be here today and I was kinda asked to talk about, um, a cardiology topic and something that's kind of near and dear to my heart is complex PC. I, and I think it's something that, um, that we do a lot of, and see a lot of now and it's changed a lot over the years and, and, and I, and I wouldn't, the way I wanted to kind of treat the next 45 minutes or so was to, um, um, talk a little bit about some of the data that's come out with PC I, that, that I'm sure many of you have seen and then sort of put that in perspective and get you some stuff to think about and then, um, and obviously show you a bunch of cases too to kind of help with these things. Um, so in regards to that is to kind of start the discussion with the ischemia trial, which I'm sure everyone's quite aware of, but we'll go over that a little bit and then I really want to focus on kind of how we do PC I and how that matters and, and talk a little bit about, um, maybe how we haven't paid attention to that in the past, hit on some complex PC I tools and then show you some examples of some of the things that we, that we've done or can do and you know, kind of how we think through these cases and then leave plenty of time for questions, thoughts, you know, stuff from, from the audience or participants. So as you guys know, ischemia came out a couple of years ago and this was a very large randomized trial that was looking at how we evaluate or manage stable coronary artery disease. And this was really meant to test a strategy, not necessarily a treatment. Um And it's kind of confusing when it comes to that part of it. But the idea was is that they took a bunch of patients, about 5000 of them was stable C ad with significant ischemia. And this was usually judged by noninvasive stress testing. Most had AC T A to exclude left main disease and they randomize these patients with a high degree of ischemia to either an invasive angiography with treatment or revascularization or they did medical therapy. And the idea being is, you know, what is the best strategy for these patients that we find do medicines work? Can we safely treat them with medicines? And if they don't do? OK, then go to a Reva strategy. Uh That was really what they were after. You can see that um most patients got PC I but a fair number of them got bypass surgery. Uh And so I always joke that, you know, we've been dealing with the idea that PC I for stable coronary arteries just doesn't work. And I, I gave the surgeons a little bit of uh adjusting because I said now you're with us, ladies and gentlemen, with the whole uh revascularization thing versus medical therapy. Um And what you can see is that a lot of patients did cross over to revascularization and a fair number of patients who had invasive evaluations didn't get revascularization. So it's a hard study because there's a lot of crossover. And as, as many people know, as the more crossover we have, the more it dilutes the effect out. But what made sort of headlines was of course, that the medical therapy works and I'll get to that in a second. This was an idea and I, and I'm gonna show this to you to get an idea of we're gonna talk a little bit about coronary physiology and how that plays into evaluations. But this was essentially what their flow was is they did ischemia on a stress test. Um If there was significant ischemia, they did ac and you can see here that if they had what looked like, you know, ischemia and a stenosis, they went right on to PC I or went on to sort of cabbage uh up here. And if they didn't have it, they, they sort of required FFR evaluation and if there was something that was less than 80% but there wasn't the area of distribution on the stress test, they required off the far. And so they, they had a sprinkling of physiology. But, but I think if you take a minute and study this and we're gonna get a little bit more at this today is we're sort of relying a lot on a stress test to tell us what to do and, and, and sort of picking and choosing when we apply physiology to these things when we know that, you know, for example, our angiogram is not a very accurate assessment, sometimes of, of ischemia uh uh for coronary artery disease, but that's what they did for, for ischemia. And you can see here that, you know, in the invasive group, a lot of them had, you know, vascularization either by cabbage or PC I and the conservative group where there was a significant difference. But you can see that in fact, there was patients that had, you know, uh a revascularization, this would have been from an unstable coronary event and incidentally, something of that nature that crossed over. And this became kind of the big headline, which was that there was really no difference in these two strategies that those who were treated conservatively at first did just as well as those who were treated with invasive procedures. And the idea here is is that medical therapy is, you know, very good at helping patients and that we don't need to jump to cath and revascularization. And that was kind of the message that was sent out. And there was all these headlines about how is PC I dead, you know, is this a waste of everyone's time and all those things? And we're gonna come back to this in a second. This information in large part in this stuff comes from. Um, I was asked a couple of years ago to, to debate Judith Hockman who was the P I of the study about, you know, how this is not proof that PC I is done in Reba, a lot of what I'm talking about today. I kind of said during that sort of debate as well. It's become more refined over the last couple of years. But this is what everyone sees. This is what everyone shows. Hey, revascularization does not change cardiovascular death or M I and even the people of this study do not necessarily agree with that statement, but that's kind of what everyone sees. And I wanted, I wanna show you over the course of the next 30 minutes about this and, and how to think about this or how we think about this in the PC I world. So here's the cases because I've been talking for a couple of minutes. So you're probably getting sick of me talking. These are two cases um uh that I've chosen that show complex uh disease. Um And you can see on the left hand, they're both severe left main stenosis in this particular patient you can see that there's a high grade lesion in the circumflex. This is the led that comes up. It's very high grade with this aneurysmal component. And there appears to be, you know, a large diagonal and led and the left main itself isn't involved or is it not as kind of tough to say over here? You can see that's high grade left main stenosis here at the bifurcation with disease kind of throughout if you notice here, this is a left dominant circulation. So almost all of the coronary circulation comes from this area in these patients. And so I'm gonna get into the history of these guys later. But this is the angiograms. And when we say complex PC I, this is what we're talking about. We're talking about heavily calcified disease, bifurcations, difficult anatomy tortuosity, all of the hallmarks of a very difficult intervention. Both of these cases have, these are all cases that came from other places to our hospital because they said there's nothing we can do. And I'll get to a minute. Both of these patients were also pretty horrible surgical candidates. So this is sort of complex PC I 2023. This is what we see on a fairly regular basis. So the how is important and this came to me. Um and I wouldn't get too caught up in sort of what I'm showing you on this study. But this idea really came to me when I, when I read this a couple of years ago and this is the idea of how to deal with left wing singing. And again, it doesn't really matter what the, what the sort of the technique is to you guys. And that's not the point of bringing this up. But what the point of it is is that this was a randomized study that took two different techniques about how to stent the left man and compare them to one another. And one was clearly better than the other. And so many times in these studies, we have PC I, yes or no. It's like taking a medication, yes or no. Did you take it or did you get it? But the problem is is that how you do PC I matters. And here's an example of that you can use the same left main stenting, you know, this, you're stenting the same left main and one technique over the other and you get better outcomes. And so we need to pay attention to this stuff. This is how it occurred to me. I think the most profound example of this is syntax two, this is a relatively older study. Um You guys may have heard of syntax one, this is where the syntax score comes from. And this is a score that um helps to analyze the complexity of coronary artery disease and gives it a score. And you know, depending on that score of surgery or, or PC I, you know, 1 may be better than the other and the original study was done a long time ago, but compared your drug learning stents to surgery in patients with complex coronary artery disease. And so they said, now, listen, how about if we do it the way that we do it now and, and even the way that this study was done, it's not exactly how we do it now, but it, it highlights some of these things. And so what they did is they took patients, they signed off on a hard team that says, yeah, I think these are, you know, acceptable for PC I. And then they did Ifr which is a measure of physiology similar to a, they did it in all intended vessels to treat and this is when they were doing the hybrid thing. So don't get too caught up on that. But the idea is we're using physiology to decide what vessels need pre vascularization. We're not just looking at the angiogram and saying, oh, that's bad. That's OK. We're using physiology and all these. Ok. So physiology supports Reva conversation. Then we implant at this time, synergy, which was the sort of next generation drug looting, stent very thin struts different polymers the best of the best. And then in this particular case, and they use intravascular ultrasound to optimize those stents, meaning we put the stent in and then we optimize them by looking inside the vessel with ultrasound to see And then of course, we did optimal medical therapy. If the vessel was not ischemic, even if it was on an angiogram that showed, hey, this is, this looks severe. If it was an ischemic, we didn't touch it, we didn't do anything with it. And so you're using physiology to decide you're putting in current juggling stents and you're using IVIS to optimize your therapy. And if you look, were they successful in that? Well, if you compare syntax one versus syntax two, you can see in syntax two, that the uh rate of physiology was significantly higher than didn't use any physiology in syntax. One, the IVIS is dramatically different. 84% versus 4.8% in that study. And then you can see CTO techniques improve and even medical therapy was better in the syntax two trial. And so that's a good sort of a good sidebar is to say that when we talk about PC I versus medical therapy, it's really PC I plus medical therapy versus medical therapy, that's how it should be. Um And this is an example of how that even improved in this clinical trial. But what about the outcomes? Did it make a difference? Well, this was um at one year, you can see that syntax two, which is the blue line showed a significant improvement in major part out uh outcomes and then repeat Reva organization. So we did it a different way. We use physiology, we use imaging, we use different stents, we use different techniques and we did better than we did before. Now, this isn't randomized comparing to that historical control. But the point is is we did it a certain way, the how of it and it made a difference. And then even at two years, you can see there's a quite a dramatic difference between the two and the outcomes that occur. And so again, supporting this point that how the, how matters and how we do this are quite substantial. Uh This is perhaps my most favorite study of this sort of how we do PC I and how that thing works. Um This was a prospective observational study. It's called defined PC I. It's a couple years old now, but it's about 500 patients. And this was done with extremely experienced operators. Most of these operators did more than 300 PC isa year, which is a lot. Um They did their evaluation, they did their stenting procedure however they wanted and then they said there was a single vessel disease. They said we're done. This is, this is perfect, this is exactly how we want it. They did a blinded then ifr so physiology after you did the PC I, and they didn't show the operators and they did this pullback which can kind of show where the change in pressure is across the whole thing. And so what did they find? Well, they found that when they did that they had about a residual ischemia rate of around 22%. So about 20% or so of the lesions that the operator said this looks great on an angiogram was still ischemic after the procedure was done. Uh It's because it was diffusely diseased and, and that's why actually not the pullback gives you information about that. And what it showed was that you had about a 30% incidence of the pressure change being in the stent that you just placed about a third proximal and a third distal meaning that there was some diffuse nature to it. So if you look here, diffuse lesion was about 4%. But a focal lesion in that area was about 18% which meant when we did PC I, we didn't do what we set out to do and we didn't do a good job. We didn't put a big enough stent in or we missed, we didn't put it in the right spot. Now, as it was mentioned, I'm a big investor, ultrasound person actually. Was you our whole group is this is kind of our stick and we, we do a lot of teaching with regards to this. And um if you've ever heard myself or doctor Singh or any of us speak, we talk a lot about this. So it comes as no surprise that we were saying, well, what's the imaging component? And they did an image routinely in this particular study? But the point is, is just doing it the way that we do it with very experienced operators saying I did a really good job. You're still leaving about 20% of patients ischemic. And so now think about that, if I do a trial like ischemia and I do those things and I'm leaving 20% of people ischemic and then looking for the difference in outcomes. How does that matter? Um So what do I mean about this? This is an example. So this is a gentleman with chest pain, moderate lesion in the right coronary artery up here of about 50 or 60% ifr was 0.74. So anything less than 0.89 is significant. 0.74 is severe. You can also see that there's some narrowings and blockages down here in the distal right coronary artery in those areas. So we did an intervention, we put a stent in and this is what we have afterwards. Ok? Look at that. Beautiful, looks good, right? Um And, and I think I've shown this to a lot of interventional cardiologists and yes, it looks great. Um I couldn't get IVIS to go in this particular case. So I said, well, why don't we just measure the post physiology? We'll just put the wire down and see, maybe we'll see if this stuff down here is bad. And I thought that's what was gonna be the problem. So I put the wire all the way down and I measured the physiology and it was 0.88 which means it was still ischemic at rest. Ok. And not terribly but still abnormal. We want that value to be more than, you know, 0.89 for sure. If we get it more than 0.93 the outcomes are actually much better. And so this is still a ischemic address. And so then I'm like, oh, it's probably this stuff down here. And so as I pulled the wire back, this is the change. So you can see the pressure changes in line and then as soon as we start to go back, it changes, change changes and then it comes back to around one. OK. So this would be up here towards the, the guide of the, of the thing. And what you'll see is is that this was actually all within the stent. So all I did is we went back and we took a balloon and we made the stent even bigger and we repeated it and we got 0.92 and this is what it looks like. So no real change on the angiogram, you're not gonna see a difference, but just by going back and ballooning that stent more and making it bigger, we made the, we made the resting ifr at the end normal. And this is getting at this defined PC I where they showed that, you know, about 30% of these was within the stent. It just goes to sizing, it just goes to optimizing your stents in PC I. Uh this is a great case. So this is a gentleman who presented with a ch a positive stress test in the inferior distribution, which means they said you have ischemia in the right coronary artery distribution or severe disease in the right only. And, and you can see this is the led that comes down here and I show this to a lot of people and they say, you know, well, there's a little bit of a blockage there of about 40 50% in the led. There's not much, there's actually a more significant blockage up here in the circumflex and other areas. So that's your problem. The led is not your problem. Look at that, that's not what your issue is. OK. So I put and Ifr wire down to measure this, this is the, um this is the um the look of it here and you can see that um this is the co registration technology, which is pretty cool. So this instead of showing you that line do to determine where the pressure drop is on this, on this vessel. And what you see is is that this led is 0.85 which is very pretty significant. And actually the whole change of it, all these dots are from this lesion right here. And so in this particular case, you took a gentleman who you thought, oh, we only have one vessel coronary artery disease, just fix that to a person that has now two vessel coronary artery disease and it involves his led. And if you think about the appropriate use criteria, your vaster organization guidelines that changes the equation a little bit as to what the best therapy is for this person. Now, it turns out you have a discussion with him and you say, hey, you know, we could do PC I and both of these, you could have bypass surgery, things like that. But the point is is that if we just relied on the angiogram, we would have missed his ischemic led. So let's say we do PC I then on the circumflex where that stress test was positive because stress tests, you know, that's, that's where it was positive. So that's the only part of his heart that's ischemic, right? And then he still has symptoms. And then we say, oh, that's a failure of PC. I see you should know, what is it a failure of PC R? Is it a failure of fact that we didn't actually fix everything we need to fix? And I can tell you after doing this for a long time, it is completely untrue that the stress test is the gold standard. And we see this sort of thing all the time where a stress test comes back, quote unquote positive in one spot. And we're doing ifr of some vessel that's clearly a scheme and the distribution of the area of the stress test is not on ifr testing. So, you know, it it is the point is is that we have to dial down on truly what is causing symptoms and not just rely on data that is not as good as, as we like it to be. Um So let's change gears just quick and talk a little bit about IVIS. And again, you know, I know I have a tremendous amount of bias of this, but I think this is definitely the way forward. Ultimate is the study to remember in this particular case, this was a prospective study, about 1400 people. They excluded sort of complex cases, experience operators in China and this is the outcome. So the top line is angiographic guided PC I and the bottom is IVIS guided. And you can see at one year and three years, the IVIS guided PC I results in a reduction in major adverse endpoints. This is target lesion failure I'm showing. But all the endpoints was positive in this study, what they did, which I think is really cool is they did um an optimal stent deployment with IVIS to sort of help people. And this is one that's used pretty often. Um These are the sort of criteria that we use mean narrow, greater than five or 90% of the distal reference segment. And that's getting at this idea of what we call an under expanded stent, which is shown here. So the stent is placed in a calcified plaque and it's crimped and it doesn't allow it to expand. And so that Luminal area is small as opposed to the ends, which are bigger. And this comes from lesion preparation and this comes from expanding that stent to the, to the the maximum amount it may have started at 9%. And here, oh look, it's much better on the angiogram. But if you see it on IVIS and see it's under expanded, that's not optimal PC I, we also look to see if there's edge dissections, which is represented here. And then we don't want to land our stents in, in a bunch of plaque as well. And this is where people used to think and where the mantra came from. If you put a bunch of long stents in, you're exposing yourself to more re stenosis. Well, that was true and it still is true to a point, meaning, you know, more stents, more chance of re stenosis. But in all of these studies, what we've shown is is that if you put longer larger stents in because you use ibis patients do better than if you don't. So this sort of spot stenting of the vessel doesn't really turn out to be a great idea and trying to trying to land normal to normal like they did on this one is, is important. And then does this make a difference? It makes a huge difference. So, even in this particular study, you can see that if they did sub O PC I, it was about the same as I did angiographic out of PC I. What was really driving the end points with Ibis was optimal PC I performed with is and really striving to get those criteria met. And if you do the event rates are much different. OK. Again, how we do it matters and using Ibis and treating to certain goals, makes a big difference. This past year, this similar study was repeated with intravascular ultrasound or OCT. This was complex patients that randomized about 1600 of them. You can see endpoint was target region failure. Most of them were intravascular ultrasound oct is optical coherence tomography. Um It was initially developed for cataract and lens stuff and then we've used it in the corners. It's, it's, it's a really fascinating and great imaging. And again, the idea is that we took complex disease sort of what I'm talking about today left main severe calcium long lesions and we randomize them. And what do you see? Again, image guided P CIA reduction in target vessel failure. There's actually a reduction in death, cardiac death in those patients who had um image guided PC I. Um And again, same sort of story. If you talk about optimization. If we optimize our, our stents with our imaging, we get an even lower event rate than if we just use image guiding without optimization. Again, how we do. It makes again another bit of data, overwhelming amount of data. Now that suggests that image guided PC I is superior to angiographic guided PC I alone. And then to sort of harp on this. Again, if you combine several studies and start looking at this idea of under expansion of stents, you can see that if we have under expanded stents or put it another way, if we have optimal stent expansion, we are reducing our event rates. No matter how you define it. There's a lot of different definitions. But even picking a different definition, if we have stent optimization, we're gonna have a much better outcome for that patient than if we don't. And striving for that is super important in when we do these cases, even hemodynamic support. So impel use um use all my cases. We used Impala impala as a implantable heart pump. Uh That really works to support uh the heart and unloaded. As we do some of these complex procedures, it allows us to do more PC I, it allows us to deal more sick patients. Low ef all of these things that we couldn't do before really have opened the doors with impala support. But even impala support has gotten better. This is looking at protect two, which was one of the bigger trials comparing Impala assisted PC I to something like a balloon pump. And you can see now protect three is our most current iteration of that and our mace and event rates have gotten significantly better in that group. Why? Well, we've used ultrasound guided access. We've figured out how to pick the patients better. We've talked a little bit more as, as a, as a group and as to how we do these cases, who do, we do them and all those things. And so the point is even simple things like putting a heart pump in, we've gotten better at that too. Uh The how of putting the heart pump in makes a difference as well. It's not just about, um, it's not just about ibis or any of these other things. So let's go back to ischemia for a second because I've talked to you all about this. And so maybe the natural inclination is, is well, well, how did they do the PC I and ischemia? And, and this is a fun activity and, and I would encourage you any time you see a PC I trial that comes out. Now, um, ask how they did it and, and try to look and find. So you usually have to go to the, you know, the supplements or something like that to find it. And what you'll see here is, first of all FFR use is only in 20% of the cases. So that, that's low. Um They did allow IFR two, they combine them together, but that's, that's low. That's not even below sort of physiology use in the community. And throughout the country is much higher. Um, so then you looked at, ok. Well, how did they revascularize patients? Well, um, they used a lot of second generation jungling stents but stent not deliverable in 5% of cases and balloon angioplasty only in 1.5% of cases. 6% or there. About, there's a little bit of overlap of not being able to deliver a stent. That's crazy. That's not, that's not something that's normal in most of our cath labs to have that issue happening. I just spent some considerable time about talking about intravascular imaging. Well, they didn't even collect that variable. So we don't even know how many people use divis and didn't and things like that. And when you point this out, they say, well, it's the standard of care, that's what we're going for. So, you know, that's that, that's not an argument because the standard of care isn't to use that. And I would say, well, but we have to compare best to best. And if you're not using imaging, we know from defined PC I that you're leaving 20% of the lesions ischemic. And we know that you're not performing a non optimal PC I compared to all those other studies I showed you. So you're not comparing the best foot forward of PC I and that's just the imaging component of it too. And so this is again, I, we may, you could have repeat this study and do the best PC I and all those things I told you maybe get the same result. I don't know the answer to that, but I do know that what you're seeing there is not what most of us do. That's not how we perform that procedure. And so how does that impact the outcomes? And how does that impact the applicability of this study to what we do? Another one came out which is a very similar story. This is Fame three. This was looking at patients with three vessels, C ad not left main cabbage or FFR guided PC I. OK. Again, looking at PC I versus cabbage using good stents, good in points, not inferiority trial. And this made pretty big news because they said look again, you PC I guys you cannot be cabbage and this time we even let you use your fancy FFR Gadget and that didn't even work for you. And it's true, it wasn't non inferior. In fact, cabbage may be superior in some of these instances. But if you again, if you look at how they did it, you go down to this thing, they actually tell you your use. 11% of the case is in PC I. And so based upon what I just showed you, I think we would all probably agree that that's not optimal PC I. And so what you're comparing is not necessarily the best foot forward for PC I compared to cabbage. Um and again, it's, it just shows you that when we talk about this, it's not one thing, it's all of it together. And that's where we get to this concept of how we perform PC I matters and the precision PC I tool kit. And these are some, just pictures of all the things that we have. So shockwave is litho, that's the idea of, you know what we've done for kidney stones. But they've applied this to a balloon to treat peripheral arterial disease and coronary disease. This is a picture of an ac si orbi arthrectomy catheter. This is rotation, arthrectomy. This is coronary road map which allows you to take a picture and project that on there and not use much diet. This is IVIS. These are different stents. These are all the things that we have. Here's the, the ifr core administration that you can layer on top of things. You can use all of this stuff together to come up with the best way of treating the patient. If you just even look at lesion preparation whenever we talk about this too, how we prepare the vessel for a stent. This is a very complicated tool kit. We have angioplasty, we have these specialty balloons that cut or score. We have laser which has been around for a very long time. We have oral arrect toy which uh works differently than rotational arthrectomy. And then we have uh lithotripsy or shock weight. You have all these choices to prepare that vessel for that? ST how do you know which one to use? Which one is better? In which case, how do you put this algorithm together to treat these things? And how often are people using these whenever they're doing complex PC I, those are all things that are important, that's all going into the soup to see how it tastes. And if we don't understand those things, you're not understanding the how of it, aside from what I just showed you about ultrasound imaging, all of those particular things, even drug eluting stents now have gotten to be the point where it's much more uh niche and, and, and diverse. These are sort of a summary of the current sort of generations of, of drug utting stents, you know, synergy um is now XD. It, it is a very thin strut. Um It comes in different sizes, but they realize that the thin struts, although it's great in some instances in other instances, it works against you. And so they came out with this niche stent that had thicker struts that was made more for osteo stenting uh or coverage of all of these areas. So again, it's trying to tailor that PC I, it's not just about putting a drug relieving stent in, but it's about picking the one that is the best treatment for the lesion in front of you along with what's the best lesion along with what's the imaging along with what's the physiology, all of this stuff comes together to give us what we need. Um Osaro or from Biron is a fantastic new stents, all of these ones have different characteristics and OSO has gotten uh interestingly enough because of its outcomes in stemming. So should there be a difference in the stent? You choose based upon stemming versus, you know, stable coronary disease? Most people would say no. But when they did studies, they showed that this oso stent was clearly superior to science. Never line the stents uh in all their age or outcomes. Why is that? Well, it probably comes to the design and this is um a micro ct of the stent struck designs and how they're put together and what you can notice about the way the osaro is made is there's a lot of crosslinking and so that mesh netting is much finer uh for that for that particular um um stent, meaning that there's less opportunity for things to collapse through that stent. And if you look here, these stent struts are a little bit more wide open as you can see here and less here. And so there may be the benefit is that when you put that in stemi, when there's thrombus and all those other things, it doesn't come cheese grating through there and cause issues and that may have nothing to do with it too. It's a very thin strut stent, it's a cro polluting a polymer same to the uh to the uh previous uh cipher stem. So there may be more to it anyway. But the idea is is that it's not just about, oh I have the stent stemi put it in there. It's thinking about what you do. So for example, I use this data for most of us at, at Wasu Barnes. Now we'll put Osiris tens in during our stem is because of this data and because we think it works a little better. So let's get back to our patients a little bit. I've kind of told you all that stuff, talked at you for a little bit. So the first guy, 52 years old cirrhosis nash was presenting in cardiogenic shock. He was being worked up for a transplant and had a positive stress test. He then sort of decompensated pulmonary edema troponins went up, he's on three pressers and he's intubated. And then this is the particular picture that he has. OK. So here you can see severe left main disease. You can see here's his led. Coming down here, there's severe disease here in the proximal led. Again, a left dominant system with a bunch of stuff around here. Um So as sick as you get multiple organs involved, you know, all those sort of things. So what do we do for these guys? And how do we approach this? So the first thing is when someone's sick who's in shock, obviously, we need hemodynamic support we start putting balloons up in the left main, there's gonna be times where there's no flow and that can cause a whole bunch of problems. So the first thing, an impala that's placed in, OK. And the impala, as we talked about, you can see here, this is a nice picture of it. This provides support. There's an inflow here that sucks blood up from an impeller and shoots it out here. And this is a 3.5 or CP. So it gives you about 3.5 L of flow. Um So that's the first thing that we did. In this particular case, you have to have appropriate bastard access and all those things for it. But that's, that's what we do here. So then um it's very calcified. So we need to ablate that. So this is uh our C si uh that I showed you before or arrect toy, this we burr through there and that actually ablates off that calcium. This is a specialty balloon that we use to inflate um in that left Maine. And then you can see after we do that, you can already see a marked improvement in that left Maine in that, in that led you can see there. OK. Then what do we do? We image? And so um this is some imaging intravascular ultrasound. I I don't say this too much. But other than just to show you this is what the pictures look like. This is a normal vessel. This is a atherosclerosis here about 12 o'clock. And that calcium you can see is that bright code that doesn't let the um, the um these stuff show through there, I'll kind of scroll through it a little bit more. Um And then the left main is here and you can see the reason why you can't see behind it is because of all the calcium. And the reason that um, that the calcium looks the way that it does is because we did that arthrectomy and we ablated it. The nice part about looking with imaging is is not only can we see that the calcium is there, but we can see that we fractured it and we can see that we modified it so that we put that stent in there. It's gonna be well expanded, we change both limbs of the bifurcation. So we understand what the circumflex looks like with respect to the left main too. Is there a severe lesion in there? Do we need to treat it? And you can see it right there? That's a very severe lesion in that in that uh circumflex left main. Um If you can see here, my pointer where my hand is, this is a calcium fracture. That's a calcium fracture. So we've appropriately uh fractured that calcium too, um not gonna get too caught up into this, but this is our stenting procedure. Uh That's our imaging that we're marking where we wanna be we check our work afterwards. Um And you can see here this is the final result there and the final results of the left main here, you can see it's nice and wide open with no issues compromising the circumflex. And this is a picture of the stent that's nice and round and open. Did we treat every little narrowing of this patient? No, we did not. But we got this guy actually out of shock extubated from the hospital, normal ejection fraction. And last time I checked, he was still being sort of waiting for a liver transplant. His liver hadn't gotten a bad enough to actually have that issue. So a success story in the sense that you know, that we, we took on this case and we were successful. But again, utilizing all these things that I told you and thinking about how to plan this case. The second one is a 78 year old lady with severe COPD and semi with an e of 20%. Um she was evaluated by the heart team and felt that she was not a candidate for surgery given her COPD. Um And so what do we do with these patients? And there's a lot of these patients that and it's, and so, so do we just say sorry, medicines? Um And, and that's where I think um we've tried to and part of the, the thing today is to show that some of these cases can be done percutaneously and we can have good results. And that, you know, that that's where we really need to, to sort of evaluate these patients for some of these complicated procedures, not everybody. And there's some patients who really medicines are better and we say we wouldn't do that, but a lot of these folks, we can't help, um, but we're not seeing them. I think that's part of the, part of the national trend is they end up at a place. Surgery says you can't have surgery. Maybe there's an interventional cardiologist there who's not as experienced with some of these complex PC I techniques. And then they say, well, there's nothing we can do and, and, and that's a shame because there is something we can do for a lot of these patients. So here's the angiogram. Again, you can see a high grade lesion in the circumflex and this disaster of a mess up here and into the proximal led. And again, so some of the stuff is the angiogram just looks horrible. Um And when we show these at conferences and stuff to everyone's like, oh, you know, type of thing. But imaging allows you to simplify a lot of these things. So the first thing we did was is we just did the circumflex. We stunted that, that was simple. We could land our stent right up to the edge of the left Maine and that's what we got and we, I did and it looked good. So that was a relatively straightforward procedure. So we do that first and then we have to take on the challenge of trying to wire this thing, which is incredibly difficult to wire. But now that we've fixed the circumflex and optimized that now we can go on to the next step. OK. Um And the next step was wiring that thing which was quite difficult to do. Um And then, um we ended up realizing that the led went here and the diagonal was there. And with imaging on the inside, we could see exactly where we maybe wanted to place that stent and come up with a plan. And so we ended up doing that, placing a stent. This is a bifurcation technique you can see here's the intravascular ultrasound afterwards. So again, we're showing you we're optimizing the stent, we're looking at it to make sure it's in a good spot to make it well expanded. What does the bifurcation look like? That's a wire, that's the stent. You can see that's into the led all of those things. And what is the final result look like? You can see that's what it looks like there and that is what it looks like here. So a marked improvement in that flow and in that left main into that led, we fix the circumflex, we left behind these things. Again, you know, the sometimes we say the enemy of good is better and trying to do too much stuff is not the idea. This lady did fantastic grief, improved symptoms, got much better with aggressive medical therapy on top of this and it was a success story. Uh She did great. So um to kind of summarize here, you know, what are the core components of complex PC I? In 2023 I think one is physiologically guided revascularization. Um You know, we can't just look at an angiogram and tell you whether or not it's ischemic or not in some cases. Yeah, sure. If it's 99% we all feel comfortable with that and if it's 20 30% that's not causing any ischemia but stuff in between, we don't know. I just was doing a case yesterday. This lady had AC T with AC TFFR uh which is uh another topic and I don't know if you guys have touched on that. I'm happy if you have time to, to tell you my thoughts on that. But AC T A um is a fantastic tool now to evaluate chest pain and CTFFR is a great tool to leverage on top of that to be able to tell moderate disease and help ferret that out. And so this lady had AC TFFR that was a little bit positive in her right coronary artery. We shot an GE gram looked like a 70% calcified lesion looks kind of bad. Her symptoms were shortness of breath and she said, I think this is all from my COPD and I said, well, maybe, but you're short of breath when you do things, how do you know it's not from your heart arteries? And so, um, we did Ifr of that and it was 0.92 0.93 and we left it. Uh And so, you know, you just don't know sometimes when you look at the ingram, what you see and whether or not it's gonna help a patient um routine intravascular ultrasound, I think is, is important to guide our therapy. I think it's a critical skill. Um I am hopeful that with more clinical trials, this will receive a more favorable recommendation in our guidelines. Um But I think it's key to performing PC I lesion preparation is important mechanical circulatory support. I showed you two cases of that today. There are times where we can do pretty complicated things where we don't need that. But that's another sort of selection. That's another variable. That's another knob to turn when you're trying to dial in these interventions. And then again, aggressive medical management, none of this stuff works in the backdrop of no medical management, especially these ones with decreased TF they all need aggressive medical management and that's really a cornerstone of, of their sort of therapies. Um That's all I have. Um I think I'm about on time or hopefully about on time. I'm happy to take questions or um stuff in the chat or anything like that. Thank you so much, Doctor Sytek. That was a great presentation. So anybody have any questions for doctors and if you don't, that's fine. You can always email me and oh, here you go. You get a lot of hassle. Insurance companies getting approval for all the technologies. Um No. Um no. Um you know, usually when the hassle is getting to the Cath lab for appropriate um stuff, it, it's not necessarily for the technologies that we use. Um they're expensive. Uh And so, you know, the hospital maybe is more the hassle sometimes when it comes to those things. Um but at the end of the day, I mean, we're there to do the best thing for the patient. And yeah, these things are expensive. I mean, an impala catheter is 20 plus $1000. Um The the shockwave balloon is incredibly expensive. So is the C si over ar and all these things. So yeah, some of these cases I showed you we spent a lot of money um in the Cath Lab but at the end of the day, um you know, when you look at most of these technologies, like for example, IVIS, it's cost savings for sure, same thing with physiology. So the routine stuff that we use all the time, it's more cost savings when you show these fancy cases and all these crazy devices, those get kind of expensive. Um but it's not insurance companies, it's usually the hospital, other questions we did have a question, just said, such an interesting presentation. Thank you. Now, you're welcome. Um Yeah, go ahead. I was gonna say, you know, does anyone have any questions about CT imaging? I, I think that it isn't really complex PC I, but, but I've had a lot of questions about that as of lately. Um Personally, I've switched to almost entire CT testing. I don't know, stress testing. Um And um the reason for that is I think the data is very good, I think, um believe it or not, it's a preferred strategy. A lot of insurance companies and top of all of that, it reduces the um normal cast in the Cath lab by about 80%. So, you know, when we send patients to get an angiogram, we don't want to have it be normal. I mean, that's great for the patient, but that's doing a procedure that's cost, that's risk all of those things. Um And so we don't like that. Um We'd like to be seeing cases that were at least doing something to evaluate something or PC I or something like that. And so by doing AC T with CT FA R based strategy, you reduce unnecessary cast by about 80% which I think is fantastic. But the thing I like the most about it is that when you get a stress test and it's normal, the patient thinks I'm good. I don't have any coronary disease, everything's fine. Well, we all know, that's not true. Um, and so when you get AC T scan and you show that there's mild coronary artery disease. You can look at that and say, see, look, see that's mild, that's mild. It's not causing you chest pain, you're fine, but you have mild coronary artery disease. And so what are we gonna do about that? And, um, we had a, I had a conversation today with the patient. Same thing. We started on a statin. She wouldn't have wanted to take a statin otherwise. But we treat her with a statin. We treat her with medicines, lifestyle modifications, all of those things. And it has a much better impact on those patients when they say, oh, I do have coronary artery disease. I don't want that to get worse. Uh And so that's a, that's a useful strategy. I am not talking about CTS calcium scoring. That's not what I'm talking about. I'm talking about coronary CT A and then CT fa far after that. So other questions or thoughts for me, you all think of something later. You're more than welcome to email me and I can forward that on to Doctor Sytek. Absolutely. Yeah. Yeah. And then my contact information. So if anything comes up ever, um please feel free to reach out. Um You know, I, I fully admit that one of the deficiencies of all of us is communicating well with, with physicians and primary care physicians in particular. So I totally get it. I try my best. But, uh, please, you know, if there's ever an issue with one of your patients or do you have questions? I'm always happy to talk about them. Um, and always happy to chat about things too. Yeah. One of the things I'll be sending out doctor Sente is a cardiology directory that, um, you know, was you compiled. So, it does have all the cardiologists and the subspecialties that they're in and then their email addresses in case these physicians have any questions. That's perfect. And you know, lots of, and there's lots of other areas where, you know, hopefully we can be helpful. And the one great thing about was you and our cardiology division is we have a lot of diverse ideas, thoughts innovations, uh and things for patients. And so, um, you know, if you need a place to start, I'm always happy to help you. And if I don't know the answer, I'll pass you on to the right spot too. I mean, you know, we don't want you guys having to play kind of this game where we're emailing a bunch of people to get your answer. That's not what we're after for you. So if there's issues or problems, you can always come to me and then I can help you get to what you need. Well, we appreciate that. Thank you. All right. Have a good day. Thank you for your attention.
