Chapters Transcript Video Atherectomy Device Back to Symposium Let's make sure this, uh, thing we still perfect. So who uses atherectomy in this room? Who's been told in this room there's no data to support atherectomy? Everybody, everybody should stand up. All right, so, a couple of years ago, we were sitting at a meeting called AMP and it was the same comment on the stage was, you know what, there's no artherectomy data. We shouldn't be using this at all. And this is also the time where our field kind of fractured a little bit, not to use that term, um after IVL on purpose, but this is the New York Times blow up on arectomy devices are inappropriate. So, you know, we were sitting there, we said, you know, I feel like I've seen a lot of atherectomy papers over the years. Why do people keep this narrative going that there's no data? So, you know, I think there's a difference between saying that maybe it's not the perfect data that someone's looking for versus whether there is no data at all. And so, I'm sitting in the back of the room and I turned to someone actually worked at Medtronic and I said, you know, we could probably do a really comprehensive review of all the literature and and try to put this myth to rest, and that became this big systematic review that we published, um, that I'm just. Gonna try to go through. Now, this is a little bit data dense and so my goal here is not for you to read or memorize any of this, but it's just to show you what's out there, to show you that there is support for your practices and then also if you need a reference for your local groups, whether it's insurance, uh, teams that you're working with for coverage or referrals, whatnot, we can, um, also send this content to you to have on hand. So, I'm gonna walk through this a little bit efficiently just so I don't put you all to sleep and then we'll go into some more interesting cases. So, OK, disclaimers here in my uh disclosures. And Doctor Dua, come on upstage. We need the expert here. This is uh uh Doctor Dua from my uh close institutional home, Mass General. We're about 3 or 4 miles across, uh, Boston from each other, the vascular surgeon. So, um, this is the evidence period, if you've ever seen an evidence period, uh, pyramid and kind of at the top, and you got to be careful. They put meta-analysis on the top. Now, just remember, not all meta analysis are the same, right? You can put a bunch of like case series into a meta-analysis and claim. In a me analysis, it doesn't make a case series now a randomized trial, but when you do meta-analysis, in particular, we used to do these only for randomized trials. We like them because it controls for some variations, either small randomized trials that you need a little bit more power to look for an end point, look for consistency across trials. That's why we kind of put them at the top randomized trials, observational studies, and then we go to case studies and kind of our anecdotal reports. So in this we really looked from green. Up we're focusing on some case studies, but mainly on observational studies. You can see the percentage of papers all the way up to randomized trials. Look at orange there. Everybody said there's no randomized data for artherectomy. Now again, these aren't large 1000 person trials. These are small trials, but in aggregate, 19 papers overall are prospective randomized trials evaluating atherectomy versus alternative approaches, and you can see overall 322 papers have been published on atherectomy to date. So when we look at all these papers, I just want to break down here, you know, it's really critical for us to know that, you know, each of these devices work differently, may be used differently, right? I typically use laser in my practice very differently than I use a rotational latherectomy device. And so we broke out here where all the data kind of supported. Now, directional latherectomy has been on the market the longest. You can see the biggest blue bubble there, 37%, but nice representation of all different. Types of atherectomy devices. And then also has made a comment, some of us might do atherectomy, PTA and do uh that end of your therapy, but we also know a lot of people use adjunctive devices whether it's drug-coated balloons, um, you know, a pair of stents, whatever it might be. And so you can see that 91% of these studies looked at some combination of, uh, balloons and bare metal stents or, or uncoated balloons. So these are all reported in the studies. OK, so let's go through some of the data here. Now, a lot of these, it's hard to get a comparative arm because a comparative arm differs for all of them. So the goal here is to show you some benchmarks of where atherectomy data align with other studies, and I'll show you some references in a moment. So on average, if you look at one year for a patient undergoing an intervention of the infrainguinal segment with atherectomy, you're going to get a patency rate around 75% across all studies supported by data more than 4%. 800 patients and you can see here that when we break it down by oh observational data might show you something different, the randomized trials, they actually show the exact same thing. You can see right around 72 to 75% between the two study types. Now, look at how this references from other meta-analyses without etherectomy. So if you look at meta-analysis of DCBA for above the knee lesions, your one-year patency rate without etherectomy is around 68%. So with atherectomy versus without, and you have to imagine the patient population in an atherectomy study is going to be much different than an IDE trial approval trial for a drug called Alu. More calcium, more complex disease, but really sitting around the same patency mark at one year for above the knee. And as we know, really kind of knocking out of the park for below the knee. 63% for pole ball loan for below the knee. We don't have DCBs yet. So just to keep in mind that I think overall when the people, when people say that Sectomy doesn't work or isn't efficacious, it's a little bit of a myth. I think that we're right on par with what we'd expect and we've seen with easier patient subsets in DCB, uh, trials. Um, if you look at this by subgroups of whether above the knee, below the knee, very severe calcium, or as you know, some of these devices work in other lesions and subsets, including those that don't have significant calcium. Across the board, you can see pretty good standard rates around that same 75% at one year. So we've mixed this all together because that's how the studies were done, but we could break out above the knee versus below the knee and then calcium severity. What about uh CLTI versus claudication? So, this came up a lot. We presented this at AMP just this past year. Now, all these studies can put whoever they want in the study. So sometimes we can't tease out all the individuals with CLTI or not. So here's a gradient from people who had no CLTI in some of these 23 studies you can see in the middle panel. There versus the far right where it's all CLTI. The CLTI population actually did quite well, but you know, smaller subset than the bigger group of patients treated. But again, we're not seeing a lot of variation. We're seeing these devices being used and getting pretty much benchmark rates at one year that are consistent across all these different patient groups. OK. Amputation. This one came up a lot also. Is this safe. There was a recent analysis from the best CLI study. Are you familiar with the Best CLI study? So that was surgery versus endovascular. So they only looked at endovascular and then they looked at people who got atherectomy versus no artherectomy and endovascular. So not randomized, just what people were using. But there was similar efficacy and then the author said maybe a suggestion towards worse outcomes with um atherectomy in that group, but it was really, uh, if you look at the details of that analysis, it wasn't really. The main population or the main finding, it was really null, but nonetheless, it's important to go back to risks. So here is non-calcified patients in these different cohorts. You can see amputation rates depend. If you're in the below the knee group, you know your CLTI, no atherectomy, you're getting around a 15% amputation rate, quite high, probably a few outliers there. But we know also in all these studies we're under 2%. And if you get into the CLTI, that's where the amputation is really minimal in the claudicins. OK, if you look by arterial segment, you can see again, BTK is the driver of any amputations. Still much less than that 15%. We're looking at 5% here in these eight studies who looked at atherectomy below the knee. And by CLTI versus uh claudicin, again, you can see that gradient increase as we go into that CLTI population as we expect. So all this is as expected. These are really reference rates for you to think about in your practices, but we've never seen harm associated with atherectomy use or a greater frequency of amputation or need for surgical revascularization because of atherectomy. Provisional stenting. So I think this is the beauty, and we forget about this because I think a lot of us feel a stent-free intervention is probably the best long-term solution for most patients, in particular young ones who know that no matter how good an intervention is, they're going to come back. And so really artherectomy, I think is a strong driver of avoiding stents if you're not planning to use them upfront. And we saw that, you know, Perra talked about the randomized trial called Disrupt pads. 3. The biggest finding in that trial was good vessel prep, in that case, intravascular lithotripsy, avoided bailout stenting by more than 10% in that procedure. So if that is your approach, if that's your style, um, I would strongly favor good plaque modification to avoid, uh, bailout or unexpected stent, and I think that was supported here. If you look in some of the newer FEMPOP trials, average ballot stenting is around 15 to 20% or 8%, and that's not even in a heavy calcification. So for instance, um, in the recent Sarona trial, which I'll show you in a little bit, which is a randomization between two DCBs is around 20%. SweedPad was another trial in Europe that was a trial looking at pclitaxel versus non-pclitaxel balloons, 42% stent rate in that trial. So, it shows you that good vessel prep can keep these numbers well under 10%. We've seen this across the board for different um lesion subsets as well as different levels of calcification. OK. The last one, I'm not gonna do too much here, but this is some device-based outcome. So we were able to break down just by classes, not by brands, directional, rotational, orbital, or laser. So you can see here directional artherectomy kind of mirrored our primary findings. Pretty good patency, low major amputation, low mortality as you'd expect, and a bailout rate around 5%. So pretty standard findings for directional etherectomy here that mirrored kind of our primary findings. And again, the most data in etherectomy right now, particularly in the US, was directional. Laser, laser did pretty well as well. You can see the TLR rates were a little bit higher, and again, in my practice, lasers a lot frequently used in uh ISR particularly. Um, some people use it in thrombotic material. So we know that the lesion subset might look different than other atherectomies and we can't control for that, but the bala stenting rates are a little bit higher in laser and that might be driven by um how you approach in stent restenosis, and we're gonna talk about definitive treatment for ISR in a few lectures here. Oral lasterectomy. So again, as we talked about, balance stenting rate was a little bit higher. I find that sometimes my practice dissection rate might be a touch higher, but very effective for very severe calcium and again, uh, a pretty standard patency loss as we saw compared to the main analysis here. I think that that is heavily skewed by the severity of calcification. Yeah, and I think that's exactly right. You can't necessarily control for all that in these meta analyses. So I think that dense calcification could be a big driver there and the rotational overall at a very good findings. So you can see low rates of patency. Lost, um, really low rates of amputation and then kind of right in that group of bailout stenting under 10%. So, you know, really we didn't see too remarkable stuff. I think some of this reflects the morphology, but really nicely supporting our devices we're using for calcific disease in particular. OK, so I'm gonna move on from the data dump. Before I do, does anybody have any questions? There's a paper that was published in JSky by me and my colleagues, um, that summarizes a lot of this dense data, so I apologize. It's hard to get through in a short talk, but, uh, hopefully you can leave your understanding that if you're. Practice is to use atherectomy are not unsupported, and there are over 300 now clinical studies that evaluated atherectomy devices, um, 19 randomized trials, um, and really we are doing stuff that are data driven here, um, but obviously it's important to put the patient first to make sure you're doing it for the right reason. Any, any comments, questions? OK, I'm gonna keep us on track then. OK. So, let's go to DCB's, uh, and again, I told you, I apologize, you're gonna listen to me for a few minutes here, but I'll, I'll try to keep us moving. Um, who uses that drug-coated balloon here? Most people? OK, good. Uh, it's funny because I, I kind of came up, uh, Kenny Rosenfeld, who ran the Levon 2 trial, which is Lutonics' um, ID was training me when, uh, that trial was going on. And so I feel like I would say I've grown up with DCBs as my standard approach. And as an interventional cardiologist, if you came to my lab and said that we're taking away all your coronary drug eluting stents, you have to go back to only using bare metal stents, we probably shut the lab down until we got them back. We don't even carry bare metal stents. Anymore. And so I would say in my peripheral practice, it would be rare that drug doesn't touch the vessel at some point, whether it's through a stent or a DCB. So I'm very driven by this and I think the data supports it. So I'm gonna try to show that to you. But, you know, we also have to recognize that we've had a few hiccups in the road and um we'll talk about that as well with the Paclitaxel safety signal and how we got around that. So, here's my case. So this was a 60 year old man. Came with right limb, wrist pain and numbness, had a history of fem bypass. I, this is like one of my first patients I saw, and this uh patient kind of got a bypass and the usual thing. He just never followed up with the surgical team. 10 years went by, he saw his primary care. He has diabetes. The primary care told him that he had diabetic neuropathy. He was walking around with a cane, and then he finally had a coronary event, and then they're like, oh, someone. Look at his legs. So then my coronary guy was like, Oh, will you see him in clinic for vascular? I said, Sure. And I look at his foot and it's just like completely ischemic, and he's been walking around like this for years and look at, I got ABIs right away and PBRs. You can see. I always tell my fellows flat line is, is no, no bueno, so no, no flow down to the foot. And, um, and this poor guy's just been like literally suffering. So we brought him quickly to the lab for an angiogram. And here's his angiogram. So a little bit of a strange anastomosis, but you can see uh touchdown, but you can see the proximal anastomosis was all preserved. You see a pretty good profunda, which is why he kept his limb on, and it just reminds you why the profunda is so important. But actually his graft was fine, but the distal portion of the graft was occluded. Um, and so, you know, after a little bit of traversing, we went down the graft, took an angled catheter, was able to cross this occlusion, um, PTatus, and that was, uh, my definitive treatment after Luketonics uh DCB here. So, I was pretty happy, no stent, really didn't want a stent. There was a little bit of proximal reflux I wanted to avoid. I don't like stenting into the graft if I don't have to. So I'm gonna go back to this, but this was, um, you know, a savior for that patient who was able to get back to being functional. And I use a lot of ibis, as you've probably heard, and I like to just show that I was nice and normal without any dissection. OK. So, he comes back years later and we get an ultrasound just for surveillance of his graft and he had some proximal graft velocity increase. So, we wanted to go back and take a look at that and you can see here, this is now, I'll give you the dates here, 3 years after and look at that Peyton. If that vessel is still preserved. And that, this is what sold me on DCBs, right? I was maybe a 25 minute intervention. Um, it was one DCB and this guy still 3 years later, it looks great. We had to tack up a little bit approximately, but this was not the problem. And so this, this is really where my practice changed. So, you know, I think one thing that we have to think about is the increasing complexity of our interventions and they revised my figure into a table here, but every time we've had increasing guidelines to look at lower extremity intervention, it started from saying, oh yeah, endovascular treatment is good for that little short lesion you're going to PTA that's, you know, 70% stenosis to now in our recent guidelines saying any inclusive disease. No matter how long, it's still reasonable to try endovascular treatments for. And so, we've really moved forward with endovascular therapy, but we also suffer still from lower rates of, of patency over the long term. We can't match what we can do with the coronary and increasing rates of amputation, and Kim McNichols did a really nice job covering this last night and we can see this curve continue to increase over time. And so this is where new tools are necessary. Now, do drug-coated balloons work? Um, I think these are really nice. So this is pooled randomized trials that compare drug-coated balloons versus uncoated balloons. And you can see across the board as you go down, the five-year data starts to get too small to be significant. But you can see how big a reduction in repeat intervention you get with a drug coated balloon, and this is across numerous randomized trials. So, no one should question whether these devices work. This is clearly more efficacious than PTA alone, and I'll talk a little bit about versus stents in a few minutes. And this is actually one of the first papers I ever read by a guy named Katsanos. This proceeds the Katsanos meta-analysis, and he published this review about how effective drug-coated therapies are. And this is a really nice gradient at 2 years for target lesion revascularization for blue is uncoated balloon, orange is barrel metal stent, gray is drug eluting stent, and yellow is drug-coated balloon. So you can see us, we've moved with our therapies forward to a drug-based approach. We've really improved TLR just even through 2 years. OK. So, um, we're going to, uh, ignore this, but I appreciate our abbreviations here, but this is just, we're gonna talk a little bit about Sky consensus guidelines later. Sorry, this really thing doesn't work well. OK. So, just to comment on the sky guidelines, right now, there is a class one recommendation for drug-coated balloons as a definitive treatment. So if you end with your DCB that is supported by our current guidelines, um, and it's the probably the most predominant use of drug-coated balloons today is for definitive treatment. OK. So, let's go through, sorry, some of these slides got changed. So, let's go through the pack of taxel analysis. Raise your hand if you've heard of the pack of Tael meta-analysis. Anybody? OK. Everybody here. OK, good. So, pack the text and meta-analysis. So, this was a very interesting study. So, this is meant to be a meta-analysis like we said. The goal is to try to stick to randomized trials. The problem with the meta-analysis was there's no restriction on whether the devices are the ones we're using today. So there are devices that have been retired, the device that never made it out of the uh the evaluation. Phase or the investigation stage, they included abstracts and not published papers and overall most studies only went to 1 year because that was the mandate to get on the FDA approval list in the US is you got to get to 1 year showing safety. No one looked at death after 1 year at this point because that wasn't a concern. So 28 randomized trials were initially included, and at 1 year of those 28 trials, there's no difference in mortality. But magically, 12 trials which did report 2-year data, all of a sudden people went from having no risk of death to a 3.5% risk of death at 2 years, which probably is one of the most toxic therapies that exist at 3.5% of people die within an additional year of follow-up, and at 4 to 5 years, it was 7%. So, when we looked at this, I, you know, it just seemed pretty outlandish to think that much harm could be caused from a single treatment with Paclitaxel, and we had all these oncologists. On stage, Vivo's leading this big vascular leaders forum in DC and they say we pump 10,000 units of Paclitaxel into pregnant women who have cancer and they do totally fine. How is a single treatment with the DCB killing at 7.5% in 5 years? So, you have to think about this with caution. This is all cause of death. There was no association with cancer or lung issue or liver issue. This was just anybody who died. But as you know, this kind of turned our world upside down for a little bit. Now, you know what happened to the US market because of this? These are some data we published, and you can see here all the different strategies. Out of 2016 when really drug-coated balloons started to take off, you can see that about 45%, it reached about 45% of the market was using drug-coated balloons in the US for fen pop lesions. And then pack thetaxel happened. My slide will work. And you can see here in red that line is vertical down. So pretty much we, we really dropped to pre kind of cats on those levels around 20% DCB and lookbook became the definitive treatment for several years, uncoded PTA. I think all of us here would agree that's probably not in the best interests of patients to leave them with a definitive treatment of uncoded PTA. So we really suffered from this, and I think now we're behind it. So this are data again for many randomized trials that had completed their follow-up now through 5 years or different periods of time. When you put all the data together, this is from Sahil Pariq, Bill Gray, Peter Schneider, Published The Lancet. There was no signal of harm because the loss to follow-up was so great in those studies before that that was driving some of that mortality signal. So we came back and we saw that in a very updated meta-analysis, we put all the complete data together, we couldn't replicate what was found in that Canano meta-analysis. We looked at this ourselves. We did this in real world data. Everybody here has probably treated a patient who's in this study. 170,000 Medicare patients, whether they were treated with drug coated blues and red or non-drug and blue, you can see no difference. Those lines are overlapped in mortality through nine years. We had 9 years of follow-up here. This was just published in the European Heart Journal. So again, we never really could replicate anything found in that canalus analysis. So in 2023, the FDA had a warning label on pclitaxel devices. Um, they reversed that label. We actually used some of our data to help support the guidelines moving forward on how to do real world data here, but it was really an important moment for all of us because we really felt like we were undertreating our patients and they were suffering because of this pause. And I will tell you that that. It was true. And when you look at what happened after the FDA panel, we saw the DCB or the reversal. We see DCBs in red start to come back up. Almost now we're back to pre-Katsanas levels in the US. PTA starts to drop it even more definitively if you go forward. But also, the other thing that's really important is people did worse during the fact that that's a controversy, so you can't see the data here. But if you actually look at amputation-free survival pre-pack the Taxol, it was uh pre uh Katsanos, it was better than post Katsanos, and that wasn't always driven by COVID because we know COVID also affected a lot of our PAD patients. So we actually did harm by pausing the world and pack the Taxol, and I, I think it's very good that we're back to where we were before in terms of treating people with these devices. Eric, one question I have on this, and I think it's a confounding variable. Is what year did Medicare change the reimbursement on DCBs down to regular balloons? Yeah, so in the end of 2017, the coverage for DCBs ended the pass through payment, and that's when also all hell broke loose because we were no longer compensated or reimbursed for using these devices. So that was a big effect, in particularly for outpatient centers which weren't qualifiers. For that payment originally, but we're never gonna get a payment which makes uptake really low. So yeah, I think that changed a lot of you unfortunately. Yeah. So let me keep going to the future now. So a couple of questions that I think still remain in Paclitaxel or just drug coated balloons in general. Um, does the dose matter? Has anybody ever thought about whether you need a high dose Paclitaxel or a low dose Paclitaxel? No. Yeah, Sean, thought about Sean, what have you, what have you thought there? You know, uh, the early data suggested that there was a benefit, but I think the excipient and how well it, it uptakes to the wall probably mitigates that. And so I, I, I think it's, it's been all over the place where some early data showed high dose data, but there's some newer data, some low dose for some of the new formulations can equal higher dose. So it's not just the pcotaxel, it's also how you deliver it to the wall and whether it's crystalline or amorphous. That's a great comment. And I think when you start getting into the newer gen, uh, DCBs like Saralius DCBs, you gotta think of them as not all are created equal. Like each one of them have a different formulary that can deliver, uh, that therapy for a different amount of time. The Japanese, if you go to Japan, they will break up all of their devices based on the concentration of Paclitaxel. So they'll show you, they'll say, oh yeah, in this case we use a low dose Paclitaxel DCB, and in this case we use a high dose Paclitaxel DCB. So I was pretty shocked when I learned that. But you know, the data probably suggests that both do very, fairly well. So this is called the Copetra, if you're not familiar. This is run by Sabine Steiner and colleagues, and what they did was they randomized patients to a low dose Paclitaxel. Uh, Platform versus a high dose Paclitaxel platform. So two commercially valuable devices head to head, and what they found, and they have data now out to 5 years that they presented at Link last year, but what they found was really no difference in most of their outcomes. Now it starts to fall apart a little bit as you get to 3 to 5 years. It's a little nuanced, but I think the main take home is that we don't really think the dose matters, but I think to Sean's point, the device does matter. And so think about that a little bit as you select what you're going to use in your practice. Other question that we've come up today, does lesion prep matter? So we talked a little bit about this with IVL. Do we need to prepare that calcific disease for drug? Does that really matter? We'll get it, it's really hard to prove, and I brought up Fabrizio Finelli. This is Fabrizio's famous slide, and I'm sorry, this, my slide's got a little bit reformatted here, but Fabrizio's comment here was patency just falls off based on calcium. If you start to look at the degree of calcium and he looks at it as a pizza pie on the top left, the more pizza pie quadrants that are affected, your patency starts to suffer. So we know that we need to do something for for calcium to make our patency better, and I think that's why I always say atherectomy makes a calcific patient look a little bit more like a normal patient. That's why we can get balance that rates lower than what we'd expect without vessel. Prep in the bottom left here, that's that randomized trial disrupt pad 3. So that was the IVL with DCB versus DCB alone and you can see, I'm sorry the text is so small here it was bigger before that there was really improved ability to reduce bailout stenting with IVL, but we weren't really sure if that improved drug uptake. That's really hard to prove. Um, and then here you can see longer term outcomes from that disrupt study that still favoring IVL and blue over. PTA. So how do I think about it? I think lesion prep does matter. I don't know if anybody wants to challenge that. I think it's hard to think that calcium would allow drug to move through it without a barrier or some sort of of of some sort of pathway to the adventitia. Remember, Paclitaxel deposits itself in the adventitia. So that has to get through the intima to the adventitia to be effective so that you don't get that um hyperplastic response or neotherosclerosis. So you got to get into the vessel wall to be effective. OK. Are DCBs as effective as stents? What would people say yes, no, maybe. I don't know, right? It depends. So this is a great trial again by Sabine Steiner, and they randomized patients to either a drug coated balloon or a stent of their choice. And you can see here in follow up there's actually no difference. They only went through one here. I think they have 2 year data that's come out. No, it's not on here, but the overall. Finding from this study was that one year you can get a stent-like result with DCB if you randomize upfront. So the upfront has to say what's your plan. If it's equipoise between DCB DES, then you get randomized to either putting in a DCB or a bare metal or DES. So no difference in this study necessarily. So I'm gonna end this section on Lutonics. Um, so we know that Lutonics um is the most uh uh studied and longest approved DCB on the market. So this really led the whole DCB revolution. Again, I was, uh, training with Kenny, who was the PI on this. Trial and you know I think the most important part is that the whole randomized trial program and prospective trial program treated over 1000 patients. We saw the IDE strongly support this. I'll show you the points in a moment. And this is what led to the first approval of the DCB in the US in 2014. You can see that this is, uh, not only one trial, it's multiple trials. So there was the early randomized trial out of Europe. There was the Levant 2, which was our trial that got approval in the US, and then there was also trial data in Japan. And if you look at the data here for Lutonics, um, you can see in both Levant 1, which is that European trial, and then also in Levant 2, which was the US trial, that we really showed significant benefit out through 12 years, and now I've been past that with Lutonics DCB over angioplasty alone. And again, these are some nice data from the global SFA registry. This is the real-world use of Lutonics DCB. Uh, you can see overall patency rate around 90%, and that also is really nice, and we'll talk about ISR in a little bit, but really show that even in complex subgroups and that you're only getting a real-world registry that you're still getting superior patency rates. OK. We're gonna skip through this. If you can move through this uh case. We're gonna go on to the next section here. This is more DCB I get back on track. OK, so enough for me. Any questions on DCBs before we move to our next talk? Published Created by
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