So Alyssa, I guess a comment from the panel. I guess the question is physiology at the level of the lemanastomosis, I guess. And that's the open question. I've been cautioned and I've experienced kind of difficult circumstances where the wire can sometimes cause kinking of the vessel. Have you guys experienced that at all? And is this something that you would routinely advise, Gautam or Yanis? That's a technical issue, but an important issue. But I haven't seen this before, but the reason I haven't seen it before is because I haven't tried that. Why? Because I don't think we have interpretable FFR values for a lema. So if I don't know how to interpret the data, then why I should do it? Can I help you with that? So let me just help you. I don't think you need a different FFR value for any individual setting in the myocardium. That is, you're measuring FFR in the LED, beyond the anastomosis, and you may have an input from the lema or from the native or from collateral. But whatever value you get at that location will tell you about the potential for ischemia and correlation with the stress testing, at least the value we have. So you don't have to say, I don't know what the value is in a bifurcated LED with three septals. It is what it is. And I think it represents the myocardial flow. So when you say the lema, not many people work across lemas because it's a fairly challenging and potentially complicated information because you may fold the lema with the wire, get pseudo stenosis, or the anastomosis may be the site or diffuse disease, which I think this was also present. So more than just pick the FFR, you have to look at the whole vessel. And I was hoping I would see a pullback, pullback pressure gradient before and a pullback pressure gradient after. Because although you did excellent work in a challenging vessel, and you used a lot of very small balloons, very short balloons, but anyway, it worked out really well. But at the end, I still don't know if the physiology was normalized in that diffuse area beyond the stented segment. So if you told me the last FFR you had was 0.88, I would have been a happy guy. But if you tell me it's 0.79, that means you got diffuse disease. So, and you know, in a bypass patient, they're very challenging clinically to come back and they'll, is my chest pain gone? Yeah, but we didn't even do anything yet. So that happens. May I add a point here, just to clarify something, also for my knowledge. We know very well that the FFR has been validated in the coronary system, where the inflow is the coronary flow. When we measure the FFR in a grafted, in a grafted vessel, then the inflow is not only the coronary flow, but it's also like a systemic flow coming from the lima. So are we sure that this FFR in a grafted vessel is interpretable? Sorry. So the input source is relatively unimportant because the myocardium doesn't know where the blood's coming from. Some from the native, some from the graft, maybe a little from collaterals. Whatever number you measure, that's what's pressurizing that location. And that tells you if you need to give more blood flow because the pressure is not sufficient, the calculation. Now, did they do stress testing or some kind of validation? What kind of validation might be done? PET scanning for all these patients, for all these regions, under all these, it's a great project for you. You got a future. But at the moment, I think you can still rely on the FFR. However, the biologic problems with vein grafts give you a different clinical use of the physiology, right? Because even though you may measure normal physiology now in a vein graft, that could degenerate tomorrow. So you have to make a different decision based on other things than just the physiology. So you're partly correct and partly not. Yeah, the outcomes of these vein grafts and other interventions, of course, are variable and higher risk. So, Dr. Alton, thank you for that case. What might seem straightforward actually, of course, opens up a huge can of worms. So, thank you. Question. A question about this case. Correct me if I'm wrong. Is this LED supplying collaterals to an occluded vein graft to the RCA, to the distal RCA? So the question is, if you do like a post-PCI FFR, and it's 0.79, would you have thought that probably CTO intervention is more appropriate in this case? The question is, and you graphically is not appealing that this lesion is gonna cause an unstable angina. So does this guy have like a large area of myocardium at risk that would you do the intervention on the LED and say, well, this is an easy intervention and I'm gonna give collateral to that RCA territory? Would you at that time say, well, even if I intervene in the LED, the flow or the pressure is still not gonna be enough to that large area of myocardium and should I do a CTO intervention? I think most of us will probably fix the easy one and see the patient gets better with more nitro, more Renexa, whatever it is. But if you can help me with this question. If you get your R down and then it's just biased and straightening the lemap, would that affect your flow when you do your, you know, FFR down? Yeah, if you have a pseudo lesion, that's definitely gonna affect both your FFR and your flow and sometimes your ibis. So, but in terms of the, you know, fixing everything CTO versus- So, you know, I think the important part that I think Dr. Curran alluded to, and I think you're alluding to exactly the same thing, the FFR is sensitive to two things. How tight the lesion is and the mass of myocardium supplied. So if you are collateralizing a CTO, your 50% lesion may produce an FFR that is lower than what it should be. So if you have a borderline FFR, let's say 0.79, for example, and you say, okay, let me fix that. You know, I've got a big collateral going to the right. Let me fix the right and redo that FFR. That's not an unreasonable approach. We have done that. There is a guy called Sachdev who has published a paper that actually described exactly what you're talking about. He fixed the CTO, redid the FFR, and he actually showed that in a lot of these cases, the FFR actually climbs back up to above the threshold.

FFR

coronary vessels

interpretation challenges

collaterals

CTO interventions