Good morning and welcome to the Skype Bifurcation Club webinar series. This is your host, Daniel Webb. We're very pleased today to have our colleagues from the Middle East Bifurcation Club join us. We specifically have targeted this series to be run every third Saturday so that we can incorporate colleagues in the Middle East and Europe to be part of this webinar series. We are very happy that the Bifurcation Club has proliferated in different parts of the world and we will invite all of them to participate in these webinar series. This is a Skype-sponsored webinar and this has been a very successful webinar for the past year. These are the disclosures. Next, please. Our moderators today are Mehrabat Al-Asnaf from Saudi Arabia and Benita Shah from New York. Panelists are Dr. Khalid Al-Shaibi from Saudi Arabia, Dr. Amir Hadidi and Dr. Habib Kamra. And the presenters today will be Dr. Al-Asnaf, Dr. Ziad Ghazal from Lebanon, and also Fadi Samaria from Lebanon, who present cases. Next, please. So this has been supported by Medtronic, the Unrestricted Educational Grant. Next, please. Thank you so much for having us. I'm super excited about this series and looking forward to hearing both Mehrabat talk about imaging as well as seeing these two cases. Maybe we can go around and sort of introduce ourselves. I'm Benita Shah. I'm an interventional cardiologist at NYU in New York. Mehrabat? Mehrabat Al-Asnaf, I'm an interventional cardiologist at King Fahd Armed Forces Hospital in Jeddah. Dr. Al-Shaibi? Khalid Al-Shaibi, I'm the director of the Cardiac Center at the King Fahd Armed Forces Hospital and the president of the Middle East Bifurcation Club. Dr. Al-Hadidi? Professor Amir Hadidi, professor of interventional cardiology, professor Amir Hadidi, professor of interventional cardiology, president of the Egyptian Working Group of the Egyptian Society of Cardiology, and the vice president of the EuroCity O'Club. Dr. Gamra? Khalid Gamra, I'm a professor of cardiology at the University of Monastir in Tunisia. All right. Well, welcome, everyone. And let's just get right into it. Dr. Al-Asnaf, do you want to get us started talking about imaging and how to make it easy in these bifurcations? Sure. So my slides are there. Can you see them? Yes. Perfect. So I'm going to try to make this quick. And, you know, it's important to note that our, I don't have any relevant conflict of interest. I think a lot of us remember the October trial that was presented at ESC in 2023 that really set the tone for the utility of intercoronary imaging during bifurcation PCIs. And then there was a meta-analysis the same year presented by Greg Stone. But although these are the two that we often quote, at least more recently, we have to remember, and I am going to go into a bit of detail with the October trial, but we have to remember that actually there's a plethora of data out there that actually looks at the role of intercoronary imaging in improving not only acute procedural results, but also major adverse cardiovascular event rates. Whether we're talking about Austin lesions, bifurcations, calcified lesions, and so on and so forth. There's a battery of these trials, including the renovate complex, ultimate, and so on. The reason I want to focus on the October trial really is because this is a trial that actually showed us step by step how operators are to be using intercoronary imaging. And the reason why is that when you actually look at the outcomes of bifurcation PCIs from the Syntax trial, the 10-year mortality was 30% compared with 19.8% in those who did not have bifurcation lesions. And then you look at the E-Ultimaster registry, again, it included over 35,000 patients. MI, target lesion, and stent thrombosis were higher in the bifurcation PCI group compared to non-bifurcation lesions. What they did in the October trial is they took 1,200 patients who were unstable angina, stable angina, and non-ST elevation of mice, but with true bifurcation lesions. And the side branch reference diameter was 2.5 or more, and randomized them one-to-one, OCT-guided versus angiography-guided. And then at two years, they looked at the primary endpoint of MACE that included cardiac death, ischemia-driven target lesion revascularization, and target lesion myocardial infarction. And you can see over here that they actually adopted intracoronary imaging in at least three different steps, but it was quite extensive. So initially, there was an OCT that was conducted to actually look at the lesion, get the appropriate measurements, reference diameters, etc. And then during the intervention, looking at post-stent evaluation by the OCT, looking at stent apposition expansion, but also looking at wire position. And then they actually, at the end, looked at everything. Now, this is, I'm just referring you to a publication that we did very recently, where we're trying to show that intracoronary imaging actually can help you when you use OCT to see if you were abluminal or not. And the reason I actually mention it is if I refer you back to the October trial, I'm going to get to it in a couple of more slides, but it was, although these were reference centers and tertiary centers with operators with extensive experience with using intracoronary imaging, there was still a significant number of patients where they didn't recognize abluminal wiring and they had stent deformation that was detected in the core lab. So when you look at the total cohort and you look at the 1,200 patients, 600 patients allocated to, as I mentioned, OCT guidance and 600 to angio guidance, the average age was about 66, 21% were women, but you clearly see the event rate was much higher in the angio guided compared with the OCT guidance and it was statistically significant. So really in patients with coronary bifurcation lesions, OCT guided PCI did in fact at two years reduce events compared with angio guidance alone. This is the publication I'm referring you to that was earlier this year, where they actually looked at the incidence of stent deformation and stent deformation was not negligible in this group. Oops, sorry, I have to come back. So it actually occurred in about 9.3% of the OCT guided cases. Accidental abluminal wiring was in 44% and guide catheter induced deformation was in 40%. So 18.5% of all cases were left main bifurcations where this happened. Abluminal rewiring was 33% in the OCT guided cases, that's 55.4% corrected by physicians in 18 out of 33, which is 54.5%. So almost half of the patients were not corrected and it was actually missed. So the two year MACE with untreated deformation was 23.3%, whereas patients where they did correct it, there was no events rates follow up of two years. So as you can see, I think the messaging here is that intercoronary imaging assesses you in identifying not only appropriate apposition, expansion and so on, but actually in the procedure itself, assisting us in figuring out what's going on. The next is the meta analysis that was presented by Greg Stone. Now this was a network meta analysis where they took several studies and what they wanted to look at was IVUS versus angiography, OCT versus angiography and IVUS versus OCT. But then they also looked at the overall effect of using intercoronary imaging, be it IVUS or OCT, to improve outcomes compared to angiography. And it included over 20 randomized trials, 12,000 patients with CCS and ACS, so that was a big number of patients, 7,000 randomly allocated to intravascular imaging, 5,000 to angiography, and they looked at events between six months and five years. And as you can see, these are the different trials that they actually ended up including. October was not included in this trial. The primary endpoint was target lesion failure as a composite of death, target vessel MI, and target lesion revascularization. And the secondary endpoints were these individual components. And the network of all these patients actually showed that compared with angiography guided PCI only, intravascular imaging with OCT or IVUS reduced events by 31%. And it was driven 46%, 20%, and 29% reductions in cardiac death, target vessel MI, and target lesion revascularization, respectively. The imaging arm reduced stent thrombosis by 52%, all myocardial infarctions by 18%, and all caused death by 25%. I mean, these are substantial numbers that I think at this point in time are untested and unequivocal. So the outcomes were actually similar for OCT and IVUS guidance. There was not significant difference when you looked at it. Remember, they looked at OCT against angio, IVUS against angio, but then they also looked OCT against IVUS, and they really were quite comparable. And this was presented by Davide Capodano during the ESC, and he actually looked at if you start adding October or Illumion to these trials and so on, you still see a significant relative risk reduction when you're using imaging compared to no imaging at all. So what this meta-analysis in particular is telling us is that whether you're using IVUS or OCT to optimize outcomes, there is an improvement in long-term prognosis of these patients. What are the implications? The routine use is going to improve long-term safety and effectiveness of these procedures, but we are going to need to weed out which lesions in particular do improve outcomes when you use intercoronary imaging. Now, the latest European Society of Cardiology guidelines that were elaborated this year, only months ago, actually really gave a 1A recommendation for the use of intercoronary imaging in complex lesions. They defined complex lesions as lesions that are long, lesions that are bifurcations, and left main. So really, those are the lesions that we should be using. And very quickly, what is it that we're doing? We're looking at MLD. In IVUS, it's pretty much the same thing, essentials one, two, three, but you're really looking at morphology. You want to look at the calcium count, determine and quantify calcification, high-risk plaque features, the length. You don't want to eyeball these things, stenting and stenting size. And remember, we take into consideration patient risk profile, and we want to know what are the procedural implications. Are we going to use plaque modification tools or not? And we need to identify landing zones. Post-procedure, we want to look at medial dissections, stent apposition, and stent expansion. And a lot of these new automated devices are actually going to give you an automated percentage that's going to tell you whether you are adequately opposed and expanded. And remember that ideally, you want to be at least over 80%, if not 90% is actually what is recommended in terms of stent expansion. And then you want to look at distal edge dissections and so on. Edge dissections, what is actionable? Not everyone is actionable. What you do want to look at is a significant dissection that reaches the intima that is longer than two. And there are different definitions depending on which you use, but generally speaking, this is what you want to see if it's longer than two millimeters deeper and reaching the intima. But bear in mind, a lot of the data that we have about malapposition in particular and edge dissections are a little skewed and biased because they were actually in patients in whom we had events. And so we went back and looked, a lot of these studies actually went back and looked at the intracoronary imaging, and it's not really sort of all-comer cases. I want to focus very quickly in the last couple of minutes with left main disease. And I know I focused a lot on OCT, but you know, IVUS is equally valuable. When you look at this distal left main, it is a Medina 111. So the distal left main is included, osteo-LED, osteocircumflex. Not only is the left main an important vessel, but it's actually got the most variability in the anatomy of the bifurcation. You have different sizes of the assigned side branch and the main vessel. So if it's the circumflex, it could be a dominant vessel, it could be a non-dominant circ. In addition to that, there's the size discrepancy. The left main LED and circumflex has the most variability compared with a lot of the other bifurcations. And so it is absolutely critical when we're using imaging, that we use imaging that not only defines the morphology and tells us how much calcification and so on, but really to give you proper measurements that allow you to decide what tools or equipment you're going to start to use. So this is based on EEL. You see a beautiful EEL over here. You see the media is very clear and NAR is nice and black. And you can go all the way along and do imaging in the left main, the circ, the LED, and determine what your diameters are. And then post-stenting, this is exactly what you want to be doing. You want to see that you've got it covered, the osteum of the left main. You want to look at all your bifurcation. You want to be able to look at your carina. So the top image is actually the second one from the left, the top one, is the carina. And you see a very nice opening into the circumflex. And you continue to look at the distal edges, whether you're looking at the LED, the overlapped segments, and so on. And so it's very critical that we do appropriate sizing. This was the exact same patient. Novel tools that we're able to use, and I do think it's important to use them, but to use them with caution because, again, it's radiation exposure. So there's the clear stent or stent boost, depending on which technology you're using. Lately, we have the GE that actually can give you these 3D images and actually can help with the wiring. And you can actually see, I can potentially see it helping in bifurcations in particular, so that in the process, before getting your IVUS or your OCT image, you can actually see where your wire is. And when you do these kinds of enhanced imaging, you see whether you're abluminal or not. So it's something that still needs to be proven, but really something out there that is probably helpful. Thank you. And I'm going to stop here and hand over to Tanvir and Benita if you want to discuss or move on to a next case. That's great. What a great summary of the data and use of the technology. So I'd love to go around the panel and talk a little bit. I feel like left-main bifurcations are its own beast, and I think there's a pretty good consensus about using imaging in both arms when we're dealing with left-main bifurcations. So maybe if the panelists could tell me a little bit about the usage in non-left-main bifurcations, how often your colleagues, your institution is using imaging. And if you could give just one tip to those who don't use imaging too much, what to focus on when they're using imaging in these non-left-main bifurcations, we'd love to hear your take-home point. I'll start with Dr. Al-Shaibi. Okay. Well, I think Nesbitt put it very nicely. I think the real utility of imaging when you're dealing with complex anatomy, so left-main certainly qualifies there. And then any other complex bifurcation, I don't routinely use it all the time in a simple bifurcation lesion where there's not much disease in the side branch. But as the lesion becomes more complex, as the disease in the side branch becomes more complex, I think as the lesion is longer, where there's a lot of fluoroscopic calcium, the more complex it appears angiographically, the more benefit I think there is by using imaging to clearly define those parameters, whether or not you need plaque modification tools and determining safe landing zones and proximal landing zones and sizing. So I think the more complex the anatomy appears angiographically, the greater the reason to use intracoronary imaging. Yes. I thank you, Mervin, for this great presentation. The most important thing is that you have non-left-main bifurcation lesions and you have left-main bifurcation lesions. Definitely in our country, in Egypt, we don't use in every case differently. But in non-left-main bifurcation, it depends on the size of the side branch and how it is significant to deal with, especially if you are comparing between provisional and to a stent strategy. This is very important, especially if you have a heavy calcium, you need a good sizing of the vessel. But definitely in left-main, we use more imaging, definitely, because always you have a discrepancy between the size of the left-main and the two branches. So this is very important to size, especially this is covering a very big area of the myocardial interfering with the high-risk patient. So the use of imaging is very important in this case. Dr. Gamar? Yeah, I agree with what was just said. I mean, left-main usually is the focus and when it is a left-main lesion, then we have to use imaging. But in non-left-main lesions, I think proximal LAD, proximal left circumflex should be the focus and where we should use imaging as much as we can because it's not widely available in Tunisia either. And stent apposition, I think that's the main concern of the operator. And that's maybe the main purpose of using imaging in that particular lesion. Yeah, so my take-home point, and I agree with all of the comments that have been made, is that if you're not doing enough imaging, my take-home point is to just do it as much as possible, because something that Dr. Alsanac had highlighted in her talk is that you see things, but that doesn't mean you have to act on it. And you really need to put the whole story together in terms of what you're looking at, intravascular imaging, what you're looking on the angiography, how does the patient look, how would you have tackled it without imaging, how does imaging change your mind? To me, that is the hardest part of imaging. I was trying to figure out what to do with the data that you've gotten. And the more you do it, the more you do it in simple elective cases, the more likely you are to have a better understanding of how to react in some of the more complex cases, and whether to react. So to me, that's my take-home point. One question from Marawat. So which cell to wire on OCT imaging? I think that's a tedious process. The Japanese, so what are your views? Because the Japanese put a lot of effort into multiple OCT runs. I wish we had an OCT camera which did not require contrast clearance, just sit there and help you wire. What is your view on that? You know, sort of towards what Benita was saying, the more you do, the more comfortable you get with the analysis of what you're doing. And I showed you that the October trial, these were expert operators who actually missed that they were abluminal wiring in a good percent of their patients. The nifty trick that I learned with OCT for bifurcations is that you do, you limit tissue elimination. And you sort of do what I showed you with the GE, the fluoro enhanced. And it actually, that actually helps a lot more to see whether you're abluminal or not. The tissue can be a little tricky when you have it in there. And the other thing is to remember that the more you do it, your team has to get facile with it as well, the setup, especially OCT and so on. And so it's critical that you get your team up to speed when you're doing it. I want to move on to Dr. Ghazal perhaps so that we can discuss it more practically through a case. And he's going to tell us a bifurcation, complex bifurcation case from Lebanon. Yes. Good morning or good evening with wherever you are in this part of the world. And thank you Tanvir for inviting us and putting all this together and thank you Mirvad. So I want to discuss with you this 89 year old gentleman who has a history of DVT, dyslipidemia, hypertension, and a history of soft tissue sarcoma, received radiotherapy in the remote past. So he presented with oppressive chest discomfort at rest and with exertion. Generally he's in good health and he's fairly functional at the age of 89. Note that his creatinine is 1.5 with an estimated GFR of 41. And he carries an ejection fraction of 45% chronically with mild global hypokinesis. So he was planned to have a cardiac catheterization, but of course we had a concern regarding his creatinine at his age. We hydrated him properly and he received the cardiac catheterization that day. And as you see, you already see that these are calcified vessels. There is an osteo LAD and there is an osteo CERC OM lesion which is quite tight. You notice also that this osteo LAD, there is a one or two millimeter length segment prior to the tight spot. But for all practical purposes, it is an osteo LAD. And you can see it here. You see, for example, let me see if I can get my laser pointer. you see my laser pointer here? Yeah. Yeah. So you can see here how there's this little ectasia just prior to the tight lesion. And of course you see here this OM bifurcation lesion. You see also the calcium in the LAD starting from the left main all the way down to the mid LAD and also the circumflex. And this is his right coronary artery. And you can see here that this is not even a very simple lesion to wire because it comes, it's sort of a lesion just before a bed. So we were expecting the wire to maybe give us some challenge. So I wanna, if you don't mind, Benita and Merva, just to bring these questions for discussion. And for example, one is revascularization strategy. The guy is 89, creatinine 1.5, fairly functional, CABG versus PCI. And if you choose PCI, what are the specific risks you should share with the patient and family? And I think that's an important question before when we do sort of ad hoc androplasty. And if you plan on PCI, should it be staged? And if staged, which vessel would you treat first? And as you, you know, deliberate, I wanna, I just wanna go through, I mean, without saying anything, I just want you to see and for the audience to see the lesions again. But go ahead and let's have some discussion. That's great. So how many of you are sending this patient off to bypass? Yes, bypass surgery. And the age of this patient, 89, is a very old patient. I don't know if all the cerebral vessels are okay. I don't know if it is okay. And because sometimes it's really in this heavy calcified lesions that you have a problem in even the cerebral circulation and the maybe high risk to do surgery for this case. Yes, if he's younger, maybe this is a case for surgery. But the problem is that we have a very high risk osteo-LAD. And I think this is our main concern now. It's a staged procedure, I think for me. Do the left first, and then another stage for the right. But the point is how to deal with this calcium. So we need to test first the osteo-LAD because if it's balloonable or not, it will define which I can do with imaging first to assess if this can be one of the plaque modification for this calcium. And then we arrange and respond according to what we will do in the osteo-LAD. And then we can check what to do because it's a very short left vein. So I think that we cannot, maybe cannot stay at the osteo-LAD. We may cover it, but we need to decide what to do in the circumflex before doing the left vein. Yeah, so you touched on some of the needs for imaging here, for sure the calcium and the assessment of the osteum of the left vein to determine length and so on and so forth, but also the patient's GFR is low and perhaps you wanna use as little contrast as possible. So that also will assist you in using ultra low contrast in a situation like this. So any tips and tricks on defining your landing zones without using contrast with using imaging alone and perhaps additional wires, how would you tackle that in this LAD? So I guess guidance would be helpful here where it'll help us with low contrast. I wouldn't say completely zero contrast, but I agree with Amr that the short left main and the discrepancy in the size, the left main is a very sort of succulent left main. When you look at that and then it just very quickly becomes two small branches, definitely wire both, protect wire both and imaging would kind of help you determine how much calcium is in that tight osteo LAD. Habib, which strategy would you adopt? Would it be a provisional strategy and what is your backup to stent strategy if you needed one? Yeah, this is obviously a highest patient and Dr. Amr was mentioning surgery, I completely agree, but I don't think that there's any surgeon who would be happy to operate on such a patient, 89 year old patient. So going to the left first, obviously, I will go to the left circumflex first and make it as simple as possible, provisional stenting obviously, stenting short stent with that left circumflex. And then we'll see what happen to that OM and then focus on the osteo LAD. Now, my prediction is that the patient will need most likely a calcium modification because it looks already a very calcified lesion and I will lose it probably in the osteo LAD because this is going to be a left main stent and it has to be optimal. So stenting the left circumflex provisional and focus on the left main LAD, it is true that this is going to be quite difficult to do because of discrepancy of diameter. But I think with imaging and trying to define the size of the left main, we will select the right stent size. These are all very nice comments and thank you very much. But would anybody start with the right just to get one easier lesion out of the way so that if we get in trouble on the left side, at least we have this very tight right opened up because that's what we decided to do. Actually, I was just going to say that, I mean, the right, some tortuosity there, but I think I'd give myself some leeway by treating that, which is a relatively straight, easier procedure to do and get an optimal result there and then bring it back for a staged procedure. And I think as Dr. Gomela mentioned, I would start by treating the circumflex because once you stand from the left main into the LAD, treating the circumflex then becomes more difficult because all your equipment would have to pass through straps. So- Yeah, we took your advice. And well, I'm saying we, because this patient happens to be my uncle. You know, nothing worse than working on a very dear family member. And so I asked my closest friend, Fadia Salaya, to be with me on the case. And we both decided to do the right first and then stage them, as Khaled was saying. It was a bit difficult to wire that right. Finally, with the Sion Black, we were able to do it and put a, let me see, oh, yeah. I was going to say, nothing about this RCA is super simple. It looks calcified, tortuous. Yeah, it's not that easy. And we had to put this AL catheter. It took more than 100 cc of dye probably to just get down there and do what we needed to do. So I'm just showing you briefly this long stand with a good result. And to make the long story short, we decided to stage them as Khaled was pointing out. We thought, let's see what the creatinine would do. By the next day, that creatinine of 1.5, and I see this all the time when we hydrate the patient, it came down to 1.3. And we planned for a stage procedure at a later date. What later date? And we thought to check the renal function. I need to remind you, Fadia and I live in Lebanon currently. And when we did this procedure, it was the day, it was a bad day security-wise in Lebanon. And a few days later, the war started. So that next planned procedure was delayed. And so my uncle presented a month later with exertional dyspnea and mild pulmonary edema. So we put it off intentionally because of the situation in the country, but he declared himself earlier. He came back with now an ejection fraction from 45% down to 25%. He had entero-apical akinesis, total akinesis. His creatinine now is 1.9. He left the hospital at 1.3, GFR 31. Troponin was elevated. There was no acute event. So he just came. He said, I've been feeling short of breath for the last few days at rest. And there was no acute changes. This is his EKG, which shows an incomplete lift bundle, first degree. And you see there are some R-wave progression. So now we have him in the emergency room. The question is to you guys, why was there a significant drop in the EF? Do you think that the LAD closed in the interim? Now, remember there was no acute event. So I don't think he had a STEMI, but if it closed, was it collateralized? And why is there a significant rise in the creatinine? Is it all contrast-induced nephropathy? And what would you do now? Yeah, these are great questions. I mean, it sounds like he didn't present acutely. So I would think anything, a little bit of high blood pressure, a little bit of a fast heart rate, a lot of stress going on externally. Anything could really, in the setting of a critical lesion, exacerbate and create a type 2 NSTEMI that results in a significant drop, especially when the lesion from the beginning was in a, supplies a huge territory and is severe to begin with. So it may not have closed. It may still be very similar, but just the stressors on top of a lot of atherosclerosis can certainly lead to it. What we worry about with the significant rise in creatinine is what is his cardiac index now doing? Is he perfusing well enough? And now you've taken, now you have not just an anatomically high-risk patient, but also potentially a hemodynamically high-risk patient. And that adds a whole other factor there. Any other comments? Yes, I think that the, okay. Yeah, go ahead. So the point is, this is my concern from the start. You have a critical LAV, which is an index conflicts. Both are supplying most of the myocardium. And the point is, whatever it is closed or reopened again, and after, because there is in the ECG, you have a QF from V1 to V3, looks to me in the ECG, I don't know. Okay. And with, the point is, this patient, to me, I would like to start with the, again, because now we have creatinine is rising, and then we have to deal with this patient, because we need to know what happened. So we need to prepare these patients with a nephrologist to assess what to do, but we need to do an angiogram again, IVAS imaging, and to see what's happening. Because the RCA, it looks so stable. I know it's critical, but the problem is, the haziness and calcium in the LAV. I think this is, we need to tackle, to assess, to improve the LAV function. Yeah, to be contrarian, if it's just one vessel I could work, we have to do in this case, that will affect longevity and prevent heart failure. I know there's multivessel disease. I always go after the LAV, because that's what gives you survival and decrease the chances of a cardiac event, heart failure. And I probably, if I were doing this case, I'd probably go for the LAV first, just because I want to make sure it's got longevity, but that gives you survival. That's my opinion. I agree with that. I would have done the same. There's a question in the chat in terms of IVAS versus OCT, and which modality would you use? I think OCT comes with contrast, and you can't, with IVAS, you want to do a pullback to try to get some exact length measurements as much as possible. Look at the bifurcation along the way, and you can minimize contrast with those IVAS. So I agree with your use of IVAS here as well. So what happened? I'm just gonna go ahead just to, only because you only have a couple minutes left. So we discussed it with the family. Now he has an EF of 25% rising creatinine. If we were to do the complex LAD and CERC marginal lesions calcified, it carries a significant procedural and renal risk. So we decided with the family, and I was part of the family, to try to optimize him medically and see if he can improve before we address his other lesions. He did well on diuresis in the hospital, and he was discharged four days in a stable condition feeling much better on home diuresis, but he was readmitted three days later with chest pain, dyspnea, and at this time, he definitely had desaturation. His creatinine was 2.2. That was four days later. So definitely he didn't like conservative management. And at that time, I took him to the cath lab. Fadi was already across town, so I was on my own. And I told my cousins that we could be facing dialysis because I was expecting things to be a bit complex. And this is how it looked. That LAD was still open, but very, very tight. And you see how there is this, I would say, it takes off eccentrically. You see this CERC marginal lesion here. It takes off a bit eccentrically in a bit of an ectatic area here, very short beyond the left main. So if you look at it here on a magnified view, the reason why I'm pointing this out is because I had a very hard time wiring it. I wanted to wire that LAD first. I knew the CERC wiring wouldn't be too much of an issue. Remember how it looked and remember the calcium. So here the question is, but I'm gonna just zoom through it, should we use a calcium modification tool? How should we approach the calcified osteo-LAD? And I think in the discussion prior to this, you guys already have elaborated on that and whether we should cover the left main or not. Whether we should place an osteal stent in the LAD versus a left main stent to the LAD. And then what's the approach to bifurcating marginal two stent technique versus provisional? So let me tell you quickly what I did. The common approach that was nicely discussed during this session is intravascular imaging. And I think Mervet really elaborated very nicely during her presentation. And of course, calcium modification technique. I didn't use any of the two and I wanna maybe use the excuse of the Eclipse trial, which just came out probably around the same time. Orbital arthrectomy versus conventional balloon androplasty prior to DES in patients who have de novo lesions with severe calcium, just like this patient identified by androgram or intravascular imaging. This was, as you know, recently released at TCT. In fact, intravascular imaging with these very severely calcified lesion was performed in only 62% in each group. And the conclusion was that the routine use of orbital arthrectomy did not improve minimal stent area or reduce target vessel failure at one year compared with conventional balloon androplasty prior to implantation of the drug eluting stent in severely calcified lesions. Anyway, I had a very hard time wiring that LAD. And you can see I ended up landing in tiny little branches. And if once I was pointing in the right direction, the wire was buckled, with buckle, use several guiders to try to orient me better, probably five different shape guiders. And even going back to a JL, finally decided to do that CERC, which actually turned out to be very easy. Both branches, provisionally stented it, looked good. Went back to the LAD, of course, with micro catheter. And we have to remember, when you use a micro catheter in such an osteo, very tight, eccentric lesion, you could close it completely. And you can't say if you're not careful, because I'm not sure how we can be careful or not careful. Which way, what? Wire, wire, which wire do you use? Yeah, so, yeah, started with the regular wire, like the run through, then the whisper, and then C on blue, C on black. Finally, what worked was I really wedged the micro catheter as much as I could carefully in a position at an angle where I thought it would be the place to take off. And then with a Gaia, one wire. So that's what basically used, what worked with an EBU 4.5. So you have to remember all of this took quite a bit of dye, changing catheters, and obviously on the table, you start getting a bit the snake pressure. We started off with 100, 110. We were a bit down to in the 90s, but finally we were able to wire it, ballooned it. And then after all of this, I decided to place the stent ostially. So forget here about imaging, calcium modification. This is a, you know, your regular multivessel disease patient who's progressing in the way that I described. It's not a stable patient sitting live to be performed live in a big conference. So, and we don't have the luxury here to use imaging. Of course we have IVUS and I can easily use it, but I thought with everything that went on, I just wanted to finally get out. So we placed it ostially, and basically it started looking good, a little bit of post dilatation. And you can see here how the stent was actually, luckily, very nicely placed at the ostium. By the time we were finishing, he was needing to be on a BiPAP. So I didn't want to put an IVUS into that lesion. I accepted the final outcome, which was angiographically very good. You see that lesion in the CERC and here in the osteo-LAD that were nicely opened. The creatinine, when he was, before that case was 2.2, I kept him in the hospital on two days watching his creatinine rising all the way to 6.45. And we were almost going to start dialysis, but then it came down. It, you know, I think it came down, not because, I mean, one of the reasons in this cardio-renal syndrome is that when we repeated his echo four days after the procedure, his EF went up from 25% to 45%. And as Benita was mentioning, maybe his creatinine initially went up also because of the drop of the EF and low perfusion. And now everything improved after we totally revascularized him. The LAD, which was, the wall, which was achinetic came back into action, EF improved, perfusion improved. And then actually two weeks ago, his creatinine was 1.3 last time we checked it. So he was back to his baseline or even a little bit better. Ben, I think amazing case, amazing case. Yes. We're gonna, that really was, and great save. And I'm glad he's doing better. For the sake of time, we're gonna move on to the next case for Dr. Sawaya. I will, while he's loading up his slides, I will mention those large left mains where the wires are buckling, they can be incredibly tiresome and frustrating to deal with. One easy trick that sometimes, like maybe has worked for me about 80% of the time is putting that second wire in the circumflex and putting a balloon over that second wire. And then when you're trying to take that first primary wire into the LED, instead of buckling so much, it bounces off of the balloon shaft that's in the circumflex, allowing you to have a little bit more directionality in the LED. It doesn't work all the time, but sometimes it does. Unfortunately, it was buckling the other way. So here, but this is a good tip in specific situations. Very good case. The use of CTO techniques in non-CTO lesions is very nice to have this case. Thank you. All right, Dr. Sawyeh. Yeah, yeah, it's fine. I figured that out. I was saying, sorry Ziad, I left you in the second part of the case. Yes, yes, you always do that. So this case is an 84-year-old female who came to our ER with chest pain, shortness of breath. It's been going on for a few days, and she came to the ER. She had a medical history of hypertension, a new diagnosis of severe aortic stenosis with a valve area of 0.9, mean gradient of 36. That was diagnosed actually at the time of the ER visit. She had a preserved ejection fraction and had other comorbidities. Let's see. It's not moving. Okay, so the EKG, you can see it here. You can see some ST depressions and the anterior leads V4, V5, V6, some maybe ST elevation and V1, V2, not benign looking EKG. So of course, we took her to the cath lab and elderly lady, very tortuous, brachiocephalic artery. First image, I directly went with the guide. Actually, I had shot the right, I'll show it later, but directly went for a guide for the left. You can see this is the first image, areocaudal. It looks like we have a distal left main lesion. And then this is the cranial view. You see you have a Medina 1-1 with a 99 distal left main, 99 osteo-LED, 99 osteo-circ, and this is the spider view. Patient was quite unstable on the table. She had marginal blood pressure, and this is the right coronary, which was free of significant disease. So if we look at this case, we have an 84-year-old lady, multiple comorbidities coming with acute coronary syndrome. She has severe aortic stenosis, and she has this Medina 1-1 configuration with the distal left main. So discussion, I think that should be talked, should we send this patient for surgical AVR and bypass? Should we do a TAVR and PCI? If we decide to do a TAVR, should we do the PCI before, during, or after? Which strategy of stenting, two stent versus one stent? If we decide for a two-stent technique, which technique in this, in your opinion, would be the best? Would you use lesion modification? And which lesion modification? Would you go for a thorectomy? You go for shockwave? And of course, imaging should be used. And would you use hemodynamic support? I think this is where we can start our discussion. All great questions. Do you have additional data before we get into the panel discussion? Just in terms of any parameters on echo or right heart cath to indicate the stroke volume index or cardiac index or what his blood pressure is, false pressure, heart rate. Yeah, so her LTO-TVTI was normal. Her blood pressure was like 100, 110. She did not have any other valvular lesions. Her PA pressure was around 45. And we did not do aortic valve. Yeah, aortic valve was 0.9 and mean gradient 36. That's helpful. So, group, what would you do? It's a very high risk procedure. Definitely, I have a severe aortic stenosis. And the valve is bicuspid or tricuspid? Tricuspid valve. So, there is a lot of discussions about to do PCI first or TAVR first. So, I think this is a very high risk procedure. You need to be ready for both. For me, I will do both in the same session. I will be prepared. And then we'll do first the left main bifurcation. And I think we test with the balloon if it's okay. You can imaging to assess if you need a lesion modification or calcium modification, whatever you see during imaging. And then this is, I think it must be very fast to cover the coronary problem and then go for TAVR at the same session. Yeah. So, for me, this is a case about planning and understanding what all of your bailout approaches are. So, obviously, we can stop and discuss and determine a great strategy. But for the sake of time, if we presume we're going for a TAVR PCI route, I want to know what the peripheral anatomy looks like. I want to know what I can do should the patient require atherectomy. And we just saw a great case where everyone said she's going to need Rota, Rota, Rota. And it turns out the non-compliant balloons were enough to fully expand without calcium modification. So, just because it looks severely calcified on angiography, imaging can help us determine whether or not we really need anything more than a non-compliant balloon or we're going to need something more. So, until we have more information, we're getting started if you're trying to minimize the risk and you cannot do, if you cannot do both in one setting, I would just want to know what all of my backup options are. Should balloons go up and the patient's blood pressure is tolerating it, that's great. Otherwise, depending on the right heart cath numbers as well, what the wedge is, what the index is, if there's any borderline lesions and I'm going up on balloons simultaneously in the LAD and circumflex, then I would have a lower threshold to consider BAB with hemodynamic support. But again, only if all the parameters suggest they're higher risk and or potentially needing atherectomy. Any other thoughts in terms of... I think, I mean, here we need to think about the whole patient. So, I'd like to know, is her presentation, I know she came with oppressive chest pain, but was it an ACS? Did she have a troponin or is this a demand cycle, which is an ACS? So, in that situation, you're sort of obliged to have, you have an unstable plaque and I think that answers the question. So, you're going to probably need to deal with the coronaries. The other question, were you able to get a CT to assess her aortic valve as far as the root anatomy, left main annulus distance, how easy would it be to reaccess? No, you didn't. I had none of this information. She came as a transfer to the ER and from the ER to the cath lab. Like I had no information. So, I mean, if it was an ACS, you're talking about an unstable plaque, I think you're obliged to treat the coronary, but maybe one thing you could do would be something like a balloon valvuloplasty and then proceed with the PCI just to give yourself some room in case the blood pressure drops or even impella support, a balloon valvuloplasty and impella and then proceed with treating the left main, the complex left main. Is the patient having ongoing chest pain during this time? Yes, he came in for like chest pain. Like his main presentation was chest pain. He was, he had dyspnea, but he came into the ER just because he was having ongoing chest pain. And still having chest pain on the table. So, you're feeling it. Yes. And if you look at the EKG, like he had systemic changes. He was stable at the admission because I thought that he's a patient is not stable. No, no. I mean, having chest pain, like ongoing chest pain, dyspnea. Only chest pain. Yeah. May I have a comment? I think the debate when you have coronary artery disease and with histoneosis, which we want to start with, the debate is still open. And in this particular patient, because the patient is coming for acute coronary syndrome, I think that we have a choice. We have to treat the coronaries first. Now, as for the previous patient, this patient is quite old and certainly highest. And although imaging and what we have discussed previously applies to this patient, I think clinical judgment is absolutely key. And what Dr. Hazel has done with the previous patient is to change completely the strategy. And instead of stenting left main LAD, he decided for precise stenting in order to make it simple and safe. I think this is a way to go for this patient, too, is to try to make it as simple as possible and as fast as possible. And they would recommend to have a staged procedure, stand the coronary first and take the patient back for recovery. I agree. If she's having chest pain and EKG changes on the table, you need to stabilize the patient from the coronary perspective and as quickly as possible. And in those cases, I have a tendency to just do as quickly as possible, a two-cent strategy in this type of a case and not really muck around too much. You could do something as whatever you feel comfortable with doing as quickly as possible, if she's unstable. So for the sake of time, if you could tell us what happened. Yeah. So just one comment. I usually decide which is causing the patient's symptoms. So I've had cases where I feel I need to do TAVR first. If somebody has critical aortic stenosis coming with pulmonary edema, I will go with the TAVR first and then I worry about the PCI. But for me here, patient came because of his coronary disease, did not present because of his severe aortic stenosis. The severe aortic stenosis just made my life more difficult, but I don't think this is the main presentation. All right. So I'll tell you what we did. All right. So of course it was difficult to cross. We had to use a micro catheter and then I had to exchange for a rota wire. I decided to go with the rota up front because I did not want to waste time with like trying to balloon multiple times, doesn't open. So I decided to go directly with our front rotablator and we went with a 175 burr after a few packs directly crossed and then we didn't do a lot of runs. So this was good. Patient was having chest pain while doing the rotablation, but overall she was stable. And then what I did, this is the injection post. I decided not to do a rota to the CERC because I did not want to lose my wire. And what I did, I started dilating. I did a left main to CERC dilation with a 3015 balloon. Then I dilated the LAD with the same or with a longer balloon, with the 3020 NC balloon. And we see there's no waste, neither in the circumflex, neither in LAD. However, it was still difficult to put a stent. So I had to put a guide liner beyond the lesion. And then we were able to slide a 3.5 by 23 Zion stent. So we were able to stent across the CERC. I was planning to go with the two stent strategy, but then I'll show you what I did. So we did left main to LAD stent. I did my first spot with the 4.012 at 18 atmosphere. And then the second part with a 4.512 balloon. So it was a 3.5 Zion, so we went to 4.5. And then I did a wire exchange. We made sure to try to be in the distal cell. And what I did then, I did a 2.0 by 12 balloon. And it's been something I've been doing a lot recently in most of my bifurcation. I avoid doing two stents. I went with a 3.520 DEB. And I went for a short stent of two 30 seconds, instead of going for the full minute and let the patient breathe. And then I did a final kissing inflation with 2.35 balloon, did a repot. And then this was the final injection. So I avoided to put another stent in the CERC. This is also the cranial view. And this is the spider view. So what we then did, I brought her back a few weeks later, and we were able to do her TAVR safely, recheck the stents and the left main and the CERC, everything was fine. And patient is now like a few months out and she's doing excellent. And in my bifurcation cases I've been doing, I don't know what's the experience of the panel, but I've been trying to avoid doing two stents if I can. And I've been using a lot of drug diluting balloon. And we've had such good results, especially for large vessels, like when we're using for circumflex, like you see, you had a 99 osteo circumflex lesion, and we had a beautiful result with DEB. Yes. Yes. I think the use of a drug balloon is very good in this case for the circumflex. And it's very nice to finish the procedure as fast as possible. It's very nice. Great case. Dr. Gamra, you have your hand up. Yeah. I would like to congratulate Dr. Saraya for this nice case. Of course, using DCB is certainly better than putting more metal in the coronary artery system. But now we need maybe more data to validate that approach. And we are doing what you are doing, but we are awaiting data in order to be more comfortable with that approach. My question to you, was the DCB used in this case before or after the kissing? I did it before the kissing. So I predilated with the NC, did the DEB. And then I left, I kissed with actually the DEB balloon. So I had another balloon, and I introduced the other LED balloon after I finished my DEB. I just have one comment regarding the DCB. I mean, the DCB, if it works, it's going to, or its benefit over a regular balloon, let's say, would be in reducing the chances of restenosis later. But you could have argued you got the same result using a regular NC balloon three, five, at least the same acute result. Because, you know, there's not going to be a difference between a regular balloon and a DCB acutely, if there's going to be a difference in later outcomes. And then the other question I have is passing a DCB through the struts of the stent. I mean, there's theoretically, the consideration of, you know, stripping some of the coating off the balloon as it goes across struts. I mean, another thing to think about, maybe. I think also the best thing, as mentioned, Dr. Khaled, that using a non-compliant balloon before using DCB, because the DCB balloon is not a good balloon, but just for delivery of the drug. So I think you must prepare the case with NC balloon before and kissing before the DCB. And then at the end, you can put the DCB with a non-compliant balloon on the other side to end the story. Yeah, we're certainly taught, you know, in the U.S. still, it's extraordinarily expensive. So we do not pull out the DCB very often. But, you know, we are taught that for it to be the last thing that we use, so that that's the drug delivery. And so that's nice that you have to at least use the drug eluting balloon in your case as well. There's a question in the chat regarding Rhoda in an MI. And I think this gets back to the first question of, do we really think it's acute plaque rupture causing an MI versus just incredible, huge amount of atherosclerosis and some instability in the setting of just a large burden of atherosclerosis rather than actual plaque rupture with thrombus. What were your thoughts there? I think the use of, as the following the algorithm for management of these calcium before using Rhoda is to test the balloon, because sometimes when you're using a balloon and you can inflate, so it gets easy to go with a non-compliant balloon before doing Rhoda, because Rhoda definitely in this scenario would increase more the slow flow, maybe the embolization. But the point is you need to test first with the balloon, but sometimes you cannot cross with a balloon. So the only option is to use Rhoda. Yeah, I mean, yes. If you look at the NGO, it looked awfully calcified. Yeah. Would it have worked with the balloon? Yes. I mean, I didn't want to have Rhoda regret, so I decided to go up front. Could I have tried with the balloon and work? Yes, it worked in the circumflex, so it could have worked in the LAD. But I think by doing rotablation at the distal left main, you also do some plaque modification on the osseum circ the same time, which that's why. Yeah, and I agree. I mean, I think unless you're seeing, for me, for my practice, unless I'm seeing a large amount of thrombus, obvious thrombus, visible thrombus, I have no problems doing rotational arthrorectomy. So there's a large amount of thrombus. One comment, you know, the osteocirc is always very difficult to treat, and I think it's because of the sheer stress and the torsion movement between the LAD and the circ. So I think DCBA will be the treatment of choice for non, let's put it this way, not long lesions, but certainly osteocirc lesions. I think that was the way to go in the future, and a lot of studies have come out, particularly from the European Bifurcation Club, supporting that concept. I think it's a great choice here for you to do the osteocirc, because the outcome between stenting and DCB may be very comparable, actually better with DCB, if you look at some of the smaller registries coming up from Europe. Yeah, I mean, we've had the DEB now for like more than five, six years we've been using it, and, you know, if you had, I mean, this patient is old, but having the restenosis and the circ, and when you have two stent technique in a left vein, it always, you know, makes things more complicated. And then when they come for the second intervention, what are you going to do? I think this, it doesn't mean that circ is not going to restenose, but at least now I have the option to put one layer of stent, I'll do a tap on the next time. I thought this was just simpler. Great. So, so, Mirvath and Benita, can you just scroll to the question in the chat to see if there's anything relevant we need to address for the audience? I think we got through the last few questions. We were talking about TAVR and Pella, BAV, Rota. I think we got through most of it. These were fantastic cases. Thank you so much. These were great, great learning points and, and so many different ways of tackling these complex cases. So just to, you know, a reminder that we're just putting all the data together and doing the best you can is, is really the most important thing. Well, thank you so much for joining us and we'll see you next time.

interventional cardiology

bifurcation lesions

intravascular imaging

OCT

IVUS

drug-eluting stents

rotablation

drug-eluting balloons

coronary artery disease

aortic stenosis