So why antiproliferatives? As we know, any time you perform balloon angioplasty on any artery vessel of the body, you're going to cause dissections. We know that. This is actually an OCT image of an SFA where you can see the markings by the asterisks where the dissections had occurred from a balloon angioplasty. And what we know, and I'm going to actually add a little bit to this diagram verbally, is that you have the acute gain. There's actually an acute recoil as well, plus there's weight loss. So ultimately, your net gain is going to be significantly lower than what you're establishing up front or what you think you're establishing up front. Furthermore, there's the coagulation cascade. This slide is borrowed from Dr. Parikh. And we know that smooth muscle cell proliferation over the course of days and months will ultimately result in more restenosis and hence the ultimate loss of net gain in the future. And we really need to emphasize the use of antiproliferative drugs to help obviate this mechanism. So there's essentially two ways that we can do to accomplish this. One, as we know, is the paclitaxels listed in alphabetical order on the right side of the screen, and then the sirolimus cohort on the left side of the screen, which are not yet on the U.S. market. And I wanted to show, actually, interestingly, the evolution of peripheral and coronary antiproliferative technologies. So the coronary is listed on the bottom here, and you can see the FDA really approved bare metal stents initially in 1994, and then the first sirolimus coronary stent was implanted in 1999. And then, subsequently, DES was approved for coronary use in the U.S. in the early 2000s. Conversely, we're actually a few decades behind in the peripheral side, right? So the FDA approved the use of drug-eluting stents first in 2012, and then approved DCB use for lower extremity interventions in 2013. The Casanos meta-analysis, as we all know, came out in 2018, and then, subsequently, many, many analyses later, we are now back to the point where we're using drug-coded technology. I want to demonstrate some of the concepts here with the case. So this is a patient who presented with breast pain. You can see his ABI is 0.6. He has no tobrachial index because the digit was flat. So we were up and over. I believe this patient actually was lost to follow-up. He refused to come back for a few months, and then eventually got enough breast pain that he came back to us. And here you can see there's actually an iliac occlusion first, and there's a little bit of iliac disease in the common, in the mid-common as well, but essentially a flesh occlusion of the external iliac. Pretty easy to cross. The fellow crossed it, so it was probably a little bit thrombotic. My criteria, as they all know, for the iliacs, if they cross it, I'm going to put in a filter in case there is thrombus. So we did do a self-expanding stent here, and you can see a wire in the internal because after we put in the stent, the internal actually got compromised a little bit, so we did go ahead and rescue the internal. So at this point, I said, should we keep going? And the fellow says yes, of course. So here we are. SFA occlusion, flesh occlusion in the proximal segment, reconstitution in the distal SFA into papiloteal artery, and you can see essentially almost three-vessel runoff. The AT is occluded in the mid-segment, but reconstitutes distally. So we went from above, we went from down below. This is actually a mother-daughter method from down below. If I'm anticipating really a fight within the SFA, I usually upfront mother-daughter a 018 CXI inside the 035 NaviCross so that I can wire escalate to an 035 Stipango GlideWire. So I typically get access pitot bareback with a micro-needle, so a pitot access kit, put either your GlideGold, or in this situation, probably the shorter steel wire first, and then exchange to GlideGold, and then do the mother-daughter system. You have to make sure that the CXI is longer, or the 018 catheter is longer than your 035 catheter that you're using, otherwise it's not going to stick out. And then you advance the system essentially to your CTO. And I did have to escalate to 035 system as I had anticipated. Here you can see in this panel, the antegrade and the retrograde are relatively far away from each other. I did reverse cart, parallel balloon, and ultimately I was able to externalize. After ballooning, I see this. So we took further pictures down below, and I see this. I knew we were going sub-entomol, because it was traveling through a looped wire method. So I knew up front what I was getting myself into. And sometimes when you take these pictures, you're kind of blown away that even within the sub-entomol space, you don't see a lot of these side sections. But in this specific case, there was a dissection. So my plan up front was actually to do drug eluting stent on the top, drug eluting stent on the bottom, where the dissection seemed to be most obvious, and then drug coated balloon in between. And that's indeed what we did, and this was the final result. So he went from an ABI of 0.6 to ABI of 0.87. Importantly, his tobrachial index improved from 0 to 0.46. I wanted to go through a little bit of data to explain why, using this case as a demonstration, why I pursue it typically the way that I do. I'm sorry, it's only one minute left. So this is a meta-analysis looking at drug coated balloons versus PTA. And just kind of real quickly, over the short as well as long term, so less than one year and then out to more than two years, DCB outperformed PTA by primary patency as well as by TLR. And when we look at drug coated balloons versus bare metal stent, also drug coated balloons do better than bare metal stents by primary patency and by TLR. When we look at the drug eluting stent versus bare metal stent, there's a trend towards favoring drug eluting stent but not meeting statistical significance. And this is midterm data, so about one to two year duration. And then when we look at drug coated balloon versus drug eluting stent, essentially equivocal. The curves really overlap a lot, even out to three years. So in general, this is a good summary slide. Drug coated balloon tends to do better, probably, and may be equivalent to drug eluting stent. All of that needs to be determined, I think, a little bit further out to really decide whether or not drug coated balloon or drug eluting stent really should be the upfront strategy. So in my lab, what I typically do is I always use the interpretive as my end goal. So in my case, usually drug coated balloon, bail out stenting as needed. My usual algorithm, drug eluting stent, if it's osteo or proximal SFA. If there's a foreseen or a pre-seen upfront need for drug eluting stent, like in this case, I usually actually just do the drug eluting stent up front. Bare metal stent, if it's within the body of the SFA, because I've already laid down my drug. Supera, if you're up against the P2 segment. And the role of text can be useful for specific segments of dissection. Thank you.

antiproliferative drugs

restenosis prevention

balloon angioplasty

drug-eluting stents

drug-coated balloons