So, here are my disclosures. They all relate to cerebrovascular disease tools, trials. This is the Buffalo team. These are our fellows, neurologists, neurosurgeons, and radiologists, and four attending dual-train neurosurgeons. And everything I say about carotids really was learned from Nick Hopkins, my mentor, who's really the champion for carotid angioplasty and stenting. So, I'll skip through a lot of this stuff so Dr. Vidal can talk a little bit more about it, but it's a substantial cause for stroke. And here's the key message for the audience that we have here, is that there is a revival of carotid angioplasty and stenting, as well as carotid endarterectomy in neurosurgery, because we are taking ownership of stroke. And I think it's really important that we engage it and embrace it so that this continues to be a strong part, an important part of the options that we offer. The diagnosis, when I see patients, carotid doppler is the best way to really screen people. And not only can you get velocities, which give you an idea of the stenosis, but you can get an idea as to what kind of plaque you're dealing with. And not all plaques are created equal. If you see a hemorrhage, this is a higher risk plaque. You should consider more regressive therapy for that. If the doppler is positive, then I typically will do an MRA of the head and neck with plaque morphology. This is done with contrast and will give you really beautiful pictures. We'll show you what the arteries look like, what the axis is going to look like, what the arch is, if there's any intracranial pathology you should be aware of. In addition, plaque morphology will show you if there's a hemorrhage or necrotic core, again, suggesting higher risk. And when we see these kinds of things, if somebody can't get an MR, you can get a CTA, and it will give you the same kind of anatomy as well, understanding the lesion, understanding access, and the best surgical route. In asymptomatic patients who have high degree of stenosis, I'll routinely do transcranial dopplers looking for silent embolic infarction. It's a simple noninvasive test you can do with the doppler study. And you're looking for a chirp. So even though the patient's asymptomatic, they're actually having silent embolic infarction. And in those who have critical stenosis with asymptomatic disease, I'll proceed with CT perfusion, which measures a lot of different things, but this is what perfusion in a highly isolated circulation looks like. And we believe there's data, as I'll show in a minute, there is cognitive decline that can be reversed by revascularization in these patients who do not have competent circle of Willis's, and I think it's an important group, subgroup of patients we should evaluate. The management options, just mentioned, ENDART, angioplasty, stenting, as well as medical therapy. With angioplasty and stenting, you can kind of do it three different ways. You can do it with distal embolic protection, proximal, and direct carotid access. I'll leave this up for Dr. Vidal. I think the medical management has certainly evolved. The question is, what's the rate of stroke in patients who are on maximal medical therapy? That is why we have a new trial called CREST-2 going on right now, because the critique is that NACET and ACSD and ACAS and ECSD all employed archaic, outdated measures for medical management. There's a lot of controversy there. Not everybody agrees with that assessment, but there's a feeling that if you employed modern medical therapy, such as what we did at Sampras, we would have much lower stroke rates. But there's some contemporaneous data to say that these high-grade stenoses should still have a fairly high risk rate, and there's data on both sides, so that's why we have ECOPOIS and we have CREST-2. But if you look at the risks that were previously known from prior studies, you had about a two-year risk of about almost 26% in the symptomatic carotid arm and about 12% in the asymptomatic arm with best medical therapy. And so this is the standard of care, carotid endarterectomy, for 60 years now. There's no question. This is a very effective treatment based on these prior trials for both symptomatic and asymptomatic. But we have also learned who is at high risk. That has medical factors, comorbidities, cardiac and others, surgical factors, recurrent stenosis, radiation and others. And in those cases, there's no question, based on SAFIRE trial, angioplasty and stenting is an excellent option. And so when we think of these options, we think carotid angioplasty is great. However, in that evolution of maybe it's an okay idea, sort of phase two stage, we had a few really radically negative trials, EVA3S, ICSS, and SPACE, all with major sort of issues that those of us who believe in angioplasty and stenting felt did not do justice to the technique. But we did learn a few things. We learned that physician experience is really, really important. We also learned that most of the strokes occur after the procedure. Two-thirds of strokes occur after the procedure. And embolic protection is really important, although there is controversy to that. My mentor who trained me, Robert Rosenwasser, didn't feel distal embolic protection was important. But this is, despite what Dr. Nanda just showed, this is the data from the actual trials done over the last 20 years. And you can clearly see there's a progressive decline in morbidity, mortality from these procedures. And this led to the CREST trial, which he briefly showed. 2,300 patients looking at myocardial infarction, stroke, and death. And this is the key data. If you looked at any stroke, the rate was 4% versus 2.3% in favor of endarterectomy. If you looked at MI, it was 1.1 versus 2.3% in favor of angioplasty and stenting. And then when you look at the actual major stroke, the major strokes were not different. It was the minor strokes which were different. The other thing we learned was it was a 10-year trial. And the complication rates in the last five years were minuscule compared to the first five years. So again, there was a learning element to this. Overall, the analysis suggested older patients were better with endart and younger patients were better with angioplasty and stenting. But that is something that continues to evolve. This was first-generation technology. And really the most important lesson, at least the way I looked at it, was that these are complementary strategies and both have their place. This is the data on actual sites from a major registry, 2,500 patients. Look at the complication rates depending on how many procedures you have performed lifetime. So this learning curve is really important for angioplasty and stenting. It's true for centers as well. Centers that do a lot tend to have lower complication rates. And it's true for a number of patients per site. So the more patients you do, the better it is. So I really feel overall these are quite complementary strategies. And the biggest issue that remains now in terms of where we go from here is this embolic risk. So embolic risk occurs at multiple site points. You can imagine you're going through a lesion. So you're crossing the lesion so you can throw debris. Then you're angioplasty-ing the lesion, you can throw debris. You're stenting the lesion, you can throw debris. And that's all embolic stroke. How do you protect that? There are two major strategies. There's distal embolic and then there's proximal embolic protection. So distal emboli, there are lots of filters that are out there. You can use them. But the problem is you need to cross the lesion to deploy one. And depending on anatomy or pore size or its apposition to the wall or tortuosity, you may not really get a good seal, resulting in embolic debris going up north. Proximal protection, on the other hand, simulates endovascularly what happens during endotrectomy. You actually arrest flow or reverse flow so nothing is going up north. And as would be expected, the trials that were done with the two systems, the MOMA and the GOR, suggested much lower rates for stroke, myocardial infarction, and death compared to any prior carotid angioplasty and stenting studies. The advantage, again, just as I said, you have protection at all stages of the procedure. Disadvantage, these are larger systems and some patients who don't have circular Willis competency can actually fail. The question is which one is safer? Well, we have a couple of smaller randomized trials which suggest much lower rates of DWI hits in proximal cases compared to distal cases. However, what I want you to note is this PROF3 trial, which has the lowest rate of DWI hits, was for this next procedure, which is direct carotid stick. So you actually make a small transverse incision at the base of the neck just above the clavicle, directly expose, cut down the carotid, there's the common, and then you directly stick this with a catheter system across the lesion and then do the angioplasty and stenting, confirm your patency with intravascular ultrasound, and you get a very good result at the end. This trial was called the Roadster trial. This showed the lowest rate of stroke, myocardial infarction, and death ever for any carotid trial, 1.4%. It was so good that Medicare actually allows reimbursement for this procedure even in asymptomatic patients. So it's fairly popular with vascular surgeons, and its risk factors are the same as the ones I discussed with angioplasty and stenting. Bottom line, I think protection is really important. Final category is that if you look, this is a study that was done categorizing when the stroke or TIA occurred during the procedure or after. So there was a sizable number of strokes that occur in the periprocedural period, but look at them. They are happening in 48, 72, and 30 days. The capture registry also demonstrated that two-thirds of strokes occur after the procedure is completed. What does that mean? Carotid stent is the final protection. So currently, we have two types of stents, the open cell and the closed cell. The open cell are the ones where the tines are not necessarily connected to each other. They allow you to adapt to curvature, but they also allow a lot of plaque prolapse, causing embolic events after the procedure. So when you look at symptomatic, we prefer to have closed cell, and there are problems with each one. Here are some next generation stents. The scaffold stent was a trial just recently completed. The paper should be published in JAX soon, where there is a PTFE lining on either side of the stent to protect from plaque prolapse. This is the confidence trial that disclosure on the National PI for, which is the SERP. It's a floor diverter type device only sized up to a carotid to allow much better plaque prolapse protection. And this is one that's not available in the U.S., but there's more trial data available called SeaGuard, which has this very fine mesh. So this fine mesh has a pore size of 165 microns. Compare this to an open cell size. So there's a lot better protection against plaque prolapse, and these are some of the examples of the different devices. And I want to show you this one quick thing. Again, it's a single small study, much safer from a procedural standpoint, but the most important thing that I loved is there was a tenfold decline in DWI hits post-stenting with this stent compared to other trials that had been done. So finally, the part of asymptomatic disease which I want to say is I think it's a very big category. I think we currently call asymptomatic if it's out beyond six months from a TIA or a stroke or discovered incidentally. But the fact of the matter is that this is a poor definition of what's asymptomatic. I think we need better patient selection. I think we need to look at plaque morphology. I showed that with you. We need to look at patency of the circular willis, looking at hypoperfusion syndromes, and TCD for emboli. So I think we still are very archaic in terms of a definition of what's symptomatic versus what's asymptomatic compared to the cardiology literature where they have much easier sort of situations. So I hear the argument that medical therapy is getting better and should not equal, but I think the counterargument is that this is continuing to get better as well, and I think we really need to look at the trial. So I'll sort of skip through the last little bit. I've covered some of this. There's clearly data to suggest there's an improvement in cognitive outcome when you treat specially selected patients, and the next step is we are moving into a phase where we are doing the CREST-2 trial, which will really hopefully definitively address this. There are two good things about the CREST-2 trial. One is that they have two separate trials in one, so you randomize based on physician preference, whether it's stenting or endart. versus medical therapy. The second good thing is as devices get approved by the FDA, they can be rolled into the trial compared to the previous CREST one where you only use the first-generation stent for the first-generation embolic. The downside of CREST-2 is that they are enrolling asymptomatic patients at 70% stenosis. I never treat a 70% asymptomatic stenosis. I wait until they get to 80% because that's been the standard for the last 15 years for trials. I think this is the way to sort of deal with it. We do every case selection in a peer review conference. We have the guys who do endarterectomy or angioplasty and stenting, in my case both, and we have our vascular neurologists who try to optimize medical therapy and make sure that patients that are being treated have really maximal medical management based on the latest guidelines. And I think it's in this multidisciplinary approach that carotid disease should be managed. And with the stroke revolution, this is a really great opportunity for us to take control of a carotid disease. Thank you.

carotid angioplasty

carotid stenting

carotid doppler

silent embolic infarctions

CT perfusion