Hello, this is Peter Kim from UTMB Neurosurgery. Today I'm going to talk about flow aversion for posterior circulation aneurysms. These are my disclosures, none of which is relevant to the talk today. So when you think about flow aversion, many of you think about these large and giant anterior circulation aneurysms with excellent outcome. Similar aneurysms in the posterior circulation can have the same outcome in principal supply, and this will be the focus of my talk today. So when I consider using flow aversion for treating posterior circulation aneurysms, these are the factors that I take into account. The location of the aneurysm, the morphology, the size, and the severity of the symptoms and the course of the patient's disease. The location I separate into four groups, into fatibo pica, into fatiobasilar junction and proximal basilar artery, mid-distal basilar artery, including the basilar apex, and the PCA. And they're really separated according to perforator's involvement. As you can see here, good neurologic outcomes can be achieved on the perforator pore area, like the fatibo artery proximal to pica, the PCA distal to the P1 segment, and these have good outcomes upward of 80%, but once involved the basilar perforators, whether that be the fatiobasilar junction, proximal basilar artery, mid-distal basilar artery, or basilar apex, the outcomes are much worse. And this, we're talking about a good neurologic outcome of less than a third of cases. So this is just to show that even for aneurysms occurring on pica, and this is a segment of pica without critical perforators, we now have excellent floor aversion treatment strategies. So this is a case where a small baby silk floor aversion device can be placed in pica to treat a dissecting pica aneurysm. And also just to support what we talked on the previous slide, so this is a very early study on the treatment of intradural fatibo aneurysm, the floor aversion. The outcomes are excellent, and most of the aneurysms went on to be completely occluded or nearly completely occluded. So this is a study on treatment of pica aneurysms. You see here 10 pica aneurysms, 8 out of 10 completely obliterated, and 2 out of 10 have a partial response. And 3 patients actually, like the case we show, have a floor aversion placed entirely into pica, and no one suffered a cerebellar medullary stroke in this series, and everyone did well on the follow-up. And apart, so we just talked about the fatibo pica aneurysms with good outcomes, and the clinical data, the same can be said about PC aneurysms that do not involve the perforation. So for example here, we have a P2-3 segment aneurysm that we treat with a FRED Jr. floor averter, again with excellent angiographic and clinical result. So here is a series from WashU, talking about PC aneurysms, and here they have an over 80% occlusion rate, again kind of supporting our thought process that post-circuit aneurysms that do not involve the perforation zone can have very good outcomes with floor aversion. So just for recap, basically I separated the location into four areas, and I would consider and be very comfortable to offer floor aversion as a first-line treatment for aneurysms on the PCA, on fatibo artery pica, whereas I'll be much more hesitant to offer floor aversion as a first-line treatment on aneurysms involving segments that are peripherally rich, such as anything that involves the basilar trunk. Next is morphology. So sacral morphology is the most common one that we see, but it's also fusiform and dissecting, and basically fusiform is when you have circumferential involvement of the artery, and dissecting is when there's a focal injury to the artery. And interestingly, when you look at the three different morphologies, fusiform is the one with the worst outcome. So it's only 71% of aneurysms achieve complete or near-complete occlusion at follow-up. And it's also the most risky one here. You can see compared to dissecting and sacral aneurysms, it has a higher major complication rate and a higher thromboembolic complication rate. So why is that? Why don't they heal? Because healing with floor aversion really requires endothelial contact or vessel apposition because healing comes from the endothelialization from the end of the normal vessel at the end into the stent and not from circling progenitor cells. So really, to have contact to normal vessel, both proximally and distally, is critical for the healing to occur. If you don't have opposition, the cells cannot come in and heal the stent. And also, in terms of the reason why they have a higher complication is because of intraluminal or intraaneurysmal thrombus, which is most commonly seen in fusiform aneurysm. A lot of the times, the thrombus are involved with critical perforators, thus increasing the risk of thromboembolic events in general and also after treatment of floor aversion. So we talked about location, the basal, the truncus, the worst. We talked about morphology, with the fusiform being the worst for healing and also the highest complications. And how about, next is about size. So this is no surprise as being proven, not just in floor aversion, but in clipping and in queruling. So basically, the larger the aneurysm, the worse outcome there is. So here, we look at aneurysm 10 millimeters or above, and it's worse, whether it be angiographic outcome, per-procedural complications, mortality, morbidity, and also retreatment rates. So this is an interesting study by Waklu and Tashna, basically trying to address the question of when should we treat. As you can see here, all the clinical outcomes, such as new deficit, 24 hours, MRS, discharge, MRS, the follow-up, mortality, they all relate to the baseline MRS. So if you look at the graph on the table on the right side, it shows it very well. If you come on board relatively asymptomatic, for example, MRS of zero, after treatment, by and large, you remain asymptomatic, mildly asymptomatic, you're at MRS of zero for most patients or MRS of one for one patient, whereas if you look at it, if you present in sicker with more deficits from the lesion, for example, MRS of three, if you're dependent, then in this group of patients, actually more than, you know, actually half the patient worsen and died. So this paper suggests that early treatment in the disease course is probably better. And in fact, interestingly, if you look at the results for this particular series, they have a complete occlusion rate of 66%, high mortality morbidity rate of 27% with 70% mortality. But if you look at the reasons, this basically summarizes the things we talked about. A lot of the patients present at MRS three to five, about a quarter of their patients have a lot of disability from the aneurysm presentation. A lot of them have either large or giant aneurysms, two thirds of them. A lot of the aneurysms are either the Fertile Basilar Junction or Basilar Shrunk. And a lot of them have the Fusiform Pathology. So again, to summarize everything. So what is the worst post-susceptibility aneurysm to treat? It's basically these large or giant, partially from both Fusiform Basilar Aneurysms. So over the past 10 years or so in treating them, I've developed some strategies with help from many others who have reported treatment of these diseases on how to deal with these large Fusiform Basilar Aneurysms with intramural thrombus and floor aversion. So I think in general, we want to use fewer devices because there's no evidence that putting more device in has better occlusion outcomes. But we know that overlapping devices can be a risk factor for thromboembolic complications. And if you have to extend the construct into the, for example, into the PCO, into the fatigueries, you can consider self-expanding stents to reduce the metal coverage and perforator coverage. So apart from using fewer device, also we should use longer device with larger diameter. The Surpass Streamline is a good example. The Surpass Streamline 550 can expand to 7.5 millimeters in the Fusiform segment because of the lower braid angles and the number of wires. With that, you can load the device, increase the braid angle, and it will expand up to 7.5 millimeters. Of course, I also recommend routine angioplasty to increase application. In terms of placement, all of this is really about the perforators. Whether you use fewer devices, you want a better application, longer devices, for the placement, of course, you're still trying to avoid the perforator. And ideally, you want to place the device below AICA if you can. Again, more on perforators, often in these cases, you have to sacrifice the contralateral fatigue artery to eliminate endo-leak. So often, there are critical perforators such as PICA, anterior spinal, posterior spinal that can come off the contralateral fatigue segment that has to be paid attention to. And obviously, you cannot include those segments. Here, next, you want to general purchase, plan a device proximally and distally on the normal vessel, really to avoid prolapse and foreshortening the Fusiform component, which can happen immediately or in a delayed fashion. And in appropriate circumstances, if there's a big sacral component, you want to consider coiling to reduce the risk of hemorrhage. And strict anti-platelet really cannot be stressed enough in testing, and we'll talk about adding anti-coagulation later on in the presentation. And like we talked about from the tachycardia walk-through experience, maybe you consider treating a patient early on in the disease. Since this treatment involves for patient astroembolics or other form of anti-platelets, if they need a shunt or if they have swallowing problems, trouble with breathing, consider a preoperative shunting trick and PEG. Otherwise, once you commit the patient to anti-platelet therapy, it's very hard to do these procedures. And even though it may not be as pretty, as useful a version, if you have good PCOMs, PCOMs can be considered to in these diseases. And the reason why we didn't want to talk about the ruptured aneurysms is because it's a completely different subject. As you can see here, for every category, dissecting fusiform or saccula, the ruptured aneurysm streamflow aversion has a much higher mortality than the ruptured aneurysms, really mainly related to the use of anti-platelet in the setting of subarachnoid hemorrhage. So we also want to kind of talk about the fate of the cover branches, of course, using floor aversion stents in the post-circulation, like the interior circulation involves jailing some vessels. So for vessels with collaterals, like the fatigued artery and the PCA, with large collaterals, the occlusion rate is much higher because the other vessel can take over, for example, the PCOM, for example. For what we'll consider end vessels, like pica, AIK, and SCA, the rate of occlusion is much smaller, but suffice to say that even in these vessels, PO collaterals can be developed over time. We mentioned a little bit about strategies about anticoagulation. So recently, we have a new protocol when we're treating these large thrombose fusiform giant basal aneurysms with floor aversion stents. As part of the preoperative medication preparation, we're adding anticoagulation to the already antiplatelet therapy. Again, the evil in this treatment comes from metabolic complications from perforators. So the hypothesis of the thinking is that if we add anticoagulation to antiplatelet therapy, it may reduce peripheral occlusion, but it does come at a price, likely increasing hemorrhagic complication, and also it may reduce the rate of aneurysmal occlusion, or it may prolong the aneurysmal occlusion. So it's really a balance between from metabolic complication and hemorrhagic complication, or maybe aneurysm occlusion slash angiographic results. So we've looked at 50 patients with basilar trunk aneurysms treated with floor aversion. In this group, 36 patients received their endoplatelet therapy, and 14 patients had triple therapy, and we found no difference in this small group of patients in the occlusion rate. So if you look at the major risk of major stroke, no person in that 14 patients who received triple therapy suffered from major stroke, whereas four out of 36 patients in the endoplatelet therapy group did, although these are small numbers, but it may suggest that the true major from metabolic risk is less when you use triple therapy and adding anticoagulation. And this is no surprise, spontaneous intracerebral hemorrhage is higher in the triple therapy group. Two out of 14 patients compared to zero out of 36 patients. So I think we still need further research to really understand if the risk and benefits are worth, if this tradeoff is worth to add the anticoagulation to our preoperative medical regimen. So I just want to end the presentation with one case to illustrate some of these principles. So here we have a 77-year-old man presented with gait instability and swallowing trouble. So on MRI here, you can clearly see a giant fusiform basal aneurysm with an intraluminal thrombus. So here is a left vertebral injection showing the sacral segment, but clearly the whole basilar is involved here. And this is the lateral left vertebral artery injection. Next I want to show the three-dimensional angiogram showing that the belly of the aneurysm is really in the proximal basilar, including the fertile basilar junction. But again, the whole basilar is actually involved here. So in this case, the patient presents with symptoms already of trouble walking and swallowing. So here we decided to treat the patient with flow aversion therapy. So here, if you look at the figure of the flow recording left side, I'm placing a device trying only to cover the lower basilar and really trying to cover the belly of the aneurysm at the proximal basilar and take it down all the way to the left vertebral artery. And here on the right flow recorder shows that I'm doing an overlapping device that covers double covering the belly of the aneurysm here. And here afterwards, balloon angioplasty to ensure that we have good apposition, distal to the belly of the aneurysm, and you can see the AI cut there. And here, of course, we'll have to go into the right side and shut down the right vertebral, otherwise we'll end the leak into the aneurysm. And here you can see that the anterior spinal artery actually comes off the right vertebral. You can see on both AP and the lateral here, there's the anterior spinal artery that goes right into the spinal canal. So here we were able to sacrifice the right vertebral artery, distal to the takeout of the anterior spinal artery. This is the AP view. You can see the anterior spinal artery here is preserved. So we put a PEG-2 prior, as we talked about, you know, it'll be hard to do this after the patient is on antiplatelet therapy, since we're having swelling problems, so we decided to put that ahead of time. He was a baseline condition immediately after the procedure. He has an aspirin, Berlintin, and heparin. Post-op day one, developed progressive right side of weakness, with MRI that's negative for aneuryschemia. His CTA was unremarkable, so we think it's probably due to swelling. Nevertheless, we kept him on triple therapy, which consisted of aspirin, Berlintin, and we added Aloquist in substitution for heparin on post-treatment day four, and his progressive improvement of his weakness and rehab after multiple infections, and again, just to say that in all honesty, these patients all go through a pretty rocky course. This is the MRI after treatment, showing no ischemia, and this is a follow-up CTA three months after, showing the occlusion of the right fatigued artery, patent, overlapping and complete obliteration of the belly part of the aneurysm. So I didn't, as mentioned, didn't go and chase after the fusiform, mid, and distal basal segment, given the perforated involvement. So in summary, I think the current device is not ideal. I think we probably need larger and longer volibertors, maybe lower mesh densities, so that we don't risk occluding the perforator. So perhaps in the future, we may even need sequential treatment of overlapping stents in a delayed fashion to control the thrombosis, and perhaps there's a role for anticoagulation to also control the thrombosis, as we mentioned. And thank you very much, and this is the end of the presentation.

flow aversion

posterior circulation aneurysms

neurologic outcomes

perforators

coiling