I'll try to get through this quickly, it has a bunch of parts to it. It's an 84-year-old woman presented with acute coronary syndrome, had a cabbage turned out because she was too frail. This is a case I'd done 11 months earlier before her instant reef stenosis event. She had severe bifurcation left main disease and severe LED disease shown here in this right panel. The mince calcium was substantial, delivery of equipment was quite challenging, and then this aneurysmal segment of the LED we knew would be incredibly painful to wire. So a little bit of how are we going to get this done, what's the safest way, the angles here were relatively difficult. You can see it's kind of an ugly Z-bend for mechanical atherectomy. So eventually we got a SU-03, which is one of our retrograde CTO wires, to go around all those bends. It's actually a really nice wire for dealing with aneurysmal segments. I think quite amazingly and somewhat irritatingly, after about four minutes of high-speed rotational atherectomy of the 1-5 burr, it just wouldn't cross this lesion. At this point, with 190,000 RPMs and multiple passes on an angle, I was starting to really become concerned about the possibility of wire fracture with moving the wire back and forth in multiple spots, trying to avoid that. But eventually it just wouldn't go through. So the options here are to downsize to a 1-2-5 burr, potentially think about switching to orbital. But eventually we just sort of called it quits and went ahead and was able to get a little bit of an expansion with a small balloon. You can see there it still has a waste in it. But eventually with a bunch of guideline or deep seeding, we were able to get an IVL down guided DK cross to the left main, extensive stenting of the LED, got good expansion and was pretty happy with this. I'll note that there were bi-osteal LED and left main calcific nodules that were seen on the IVL. But despite that, the stents had a little bit of a D-shape to them. I just have sort of the cross-section here of the final IVL from the distal segment of the LED proximal. We had really big areas. And met the post Excel MSAs that we would want for a patient like this. And so we're pretty happy with how things turned out. And unfortunately she came back 11 months later with a non-STEMI. And this is the angiogram from her re-presentation, landed back at our hospital. And you can see she has focal and stent re-stenosis in this portion down here. And there's something funny going on in the left main and LED bifurcation with the circumflex. I took a magned view here. And you know, I should know better. Anytime I sort of mag up and do another angiogram, it means I should just stop and use imaging catheter which eventually I did. And so effectively, you know, in this scenario, this is the OCT of her left main to LED on the left. And this is the OCT of her left circumflex. The co-registration is not adequate. But I pulled out the frames that were important. And so as outlined, this is a patient that had calcific nodules in her left main bifurcation in both limbs. It was larger in the circumflex. And now 11 months later, in addition to having LED mid-segment ISR, she has stent failure where the nodular calcium is. And so, Evan, take a look at these. I'd love to hear your thoughts on it. I showed you my IVAS from the first case. We had great expansion. And so this is what I'm dealing with now 11 months later. Yeah. And it's so frustrating when you see this. And that's it. With calcific nodules, it's very common. We've seen the same thing on serial imaging. We get great final intravascular imaging where we're patting ourselves on the back. And then somewhere in the 3 to 18 months later, they come back to the lab and the nodules right where you left it, you have a pretty significant lesion. So I think we're still in the early stages of learning what the best approach to treat it the first time to really try to prevent it from coming back. To me, here, you've proven you can deliver an imaging catheter. Aside from just evaluating the mechanism, I think with this calcium and the fact that you've successfully delivered OCT, my lesion modification tool would be IVL. Yeah. That's what I thought too. The thing about this, and I always struggle, to Ron's earlier point, did I have stent scaffold failure? The nodule pushed my stent back in. Did I have nodular regrowth or did I have stent fracture? Those are the three main things that are in the differential when these fail. And the hard part is because the nodular stuff grows back into the stents in a way that neither IVS nor OCT tell you. I'm always wondering which of those three it is, and you kind of treat it the same way, but it's often a combination of both. The struts can be folded on themselves. You may, fluoroscopically, with stent boost or some other technology, see that you have fracture, and then you've just got nodules that grow back in through the stent struts. It's a little tough to tell. Doesn't matter so much, but the one thing to Ron's point, and I'd be interested, this entity that I've highlighted in this bifurcation left main failure, this doesn't usually respond well to angioplasty alone. It's one of those painful bifurcation ISR scenarios where I balloon these things, they still look awful, and very reluctantly I end up needing to re-stent. And I'll show you how I dealt with this, but I'd really love the expert faculty's comment on re-stenting this scenario or not, because that's something that I've struggled with. This is the algorithm that Evan and I developed for Optimal a couple of years ago, and it just sort of highlights the root cause with intravascular imaging. Is calcium present or not? Is the stent well-expanded or not, and is there stent fracture are the three main questions. And then we really escalate through the therapies which have been outlined, balloons, shock wave or laser or laser on contrast, drill out the tissue or drill out the stents with orbital eroda, and at the end of the day, we want to make sure we've got good expansion. And then after that, as was highlighted by Khaled, once it is well-expanded, that's when you apply some antipollutant therapy, either drug-coated balloon or brachytherapy as previously mentioned. And sometimes you have to re-stent these, and the reason why I chose this case is this is an entity where I struggle a little bit. And so, you know, once expansion is confirmed, when do we tend to consider putting another stent in? If we have big, new animal dissections, if we have stents that won't sort of scaffold the artery or stent fracture, those are the times when typically I'm thinking you're going to need to put a new stent in potentially. And so in this particular case, I actually staged this because we started this later in the day. I dealt with her mid-LED stent with IVL because the expansion wasn't perfect there, despite the fact it looked okay in the initial case in the IBIS I showed you. And then we just took a DCB approach, and to Ron's point earlier, this case is getting expensive already, right? It's an inpatient. I've used an IVL in the mid-LED. I'm treating the distal outflow native disease unstented with a 2,5 agent. I'm treating the mid-LED ISR with a 3,0 agent and try to save my boss a little bit money in a very off-label way. I took a 4,040 ranger DCB, which is the peripheral DCB, and I used that for the proximal LED. And at that point, I stopped and figured I would tackle the left mane, and we brought her back to do that the following day. And so I showed you what the entity was, and I think much like Evan suggested, we were able to deliver. So there is a value proposition to shockwave with its mechanism of action, fracturing the base of these nodules and softening them back up. You could take a 2,0 rotobur and drill it out or buy osteoorbital. Those are reasonable for debulking, but the problem here is that you need a lot of pulses to deal with these things. So I actually used two 4,0 IVLs, one balloon in the LED and one in the circ, because these tend to be relatively pulse-intensive problems. And so with that in mind, we still had recoil of both osteo and geographically. So it wasn't ready for DCB at this point in my mind, and I ended up painfully just re-coulot stenting them with two Megatrons because they're high radial force stents. You can see couloting left mane to LED and left mane to circ and flex because the recoil was quite substantial, both angiographically and on the subsequent IVIs. We did IVIs-guided stenting, made sure we had post-Excel hang criteria, superior areas and all this. It expanded quite nicely, but I sent the poor lady home thinking, we did a reasonable job the first time. I did a reasonable job, I think, the second time. What are we left to do? So in cases like this, we'll typically try to attack the inflammatory process. We gave her silostazole and colchicine because there's a little bit of data for these drugs post-intervention targeting the inflammatory pathobiology that drives this stuff. But this was a pain point for me because we tried to do a good job. We had osteostent failure in both osteo related to nodules, and it wasn't responding well enough to angioplasty that I had to do this to it. And so I'd love thoughts from the team in terms of if you have any better approach to this because I had to do exactly what I didn't want to do, was re-bifurcate stent the left mane. Yeah, it's a tough one. But if you have a stent fracture, I think you're left with no much options. You really have to re-stent it because you don't want to leave a fracture stent. Think about the mobility of the artery, the pulsatility of the artery when you have like a needle poking all the time, the neo-intima, it's like the epitome of stimulation, more neo-intima formation. So you really don't want to be in a situation like this. I would say that you have a stent fracture, what you really need to do, and you did it, if you IVL it, you work a little bit on the underlying cause, you may try to prevent a recurrent stent fracture. And that's probably would be the best, but I would never leave a stent fracture without another layer of stent. You have to do that. And I'm not such a big worry about multiple layers of stent obstructing the lumen. Remember, we have a lumen of about 3.5, 4.0, even a 3.0. So what is another 80 micron? I mean, it's really, people are afraid to do it, but I'm more afraid to leave a fracture stent undercover. Yeah. And we had huge areas at the end, you can see, so I think that part of it will be covered, but then we try to attack the inflammatory part of this. But nodular stent failure and bifurcations is a pain. They live in the circumflex and they're one of the main reasons that we see our left main bifurcation PCIs come back with stent failure. I think what I would do with this patient, hold on just one second, Evan. I would bring this patient in three months to a surveillance angiogram and imaging. And if I see that there is some tissue progressing into this area, I would add brachytherapy to this vessel because I think that just doing it and waiting for luck, it's too much. I mean, you really need to look at those patients probably in a surveillance between three to four months before they develop something, that situation that you won't be able to treat. So brachytherapy, not immediately, but in three, four months probably would be advisable here. Yeah. And we, Ron, for some of our more calciter patients have been taking to both DCBing and repeat breaking if there were prior brachyfailure because these poor people just keep coming back and back. And at least in our experience, we've had no hazard of that. We did up to three times with no hazard. As long as there is a one-year interval between the two. Yeah. Us too. We see a lot of this. Devin, you were going to say something? Yeah. I was just going to ask the panel, would you guys start any role of different strut, either thicker struts, scaffold or something more supportive? Some thought of potentially like a Megatron for these calcific nodules, perhaps to prevent some of that potential recoil that there's. Yeah. I use a thin strut stent in nodular calcium and that's why I chose Megatrons to retreat as the buttressing capacity is touted to be superior. I'm glad that you brought up that pharmacotherapy. I think pharmacotherapy is critical here and I would just go beyond. There was a question about P2I12 non-responders with the imaging. If you see there's no thrombus, I don't think that's really the driving factor here. Anytime I see neo-atherosclerosis with instant restenosis, I'm very aggressive with getting that LDL below 55, very liberal use of PCSK9 inhibitors in addition to the anti-inflammatory meds that Kevin talked about.

coronary artery disease

intravascular lithotripsy

stent failure

calcific nodules

recurrent restenosis