Chapters Transcript Video CTO & Complex Intervention Dr. Paul Lavigne describes chronic total occlusions and the recommendations to revascularize to improve symptoms. I'm gonna touch upon a little bit of data and then show some cases uh uh about what may you know, kind of uh demonstrate how CTO PC I may differ from conventional PC I and what we look for in both case selection and and uh and procedural approach. But uh to define chronic total inclusion is important. So we're looking for 100% inclusion in the coronary artery with non collateral to me, zero flow of at least three month duration. Uh duration may be difficult to ascertain by looking at an angiogram. So we often use the uh clinical estimate of symptom duration as a surrogate for that. And it's highly prevalent among patients undergoing diagnostic angiography in some case series up to almost a third of patients um have CTO S and it's important to differentiate a CTO from persistent inclusion after a recent AMI where we know revascularization can have some uh untoward outcomes based on things that we've learned from uh the O trial and some uh former, former uh data collection CTO S cause ischemia, even with well-developed collaterals is demonstrated by a variety of imaging and uh hemodynamic modalities. SPECT CFRFFR and they're associated with higher rates of death and non-fatal adverse cardiovascular events in various populations. We know in A CS patients with non culprit, CTO lesions, they have worse outcomes compared to those with uh either single vessel involvement or multivessel, non chronically included lesions. And this is also true uh in shock patients as well. So when we're looking at the guidelines to help direct what we need to do with patients who have chronic total inclusions, we're looking at patients with stable ischemic heart disease and we know that the most strong indication for revascularization in this population that CTO or otherwise is to alleviate symptoms in patients who have refractory symptoms on appropriate medical therapy. There may also be a role to improve or hard outcomes like cardiovascular death or acute M I in patients with select uh characteristics. And when you look at CTO S specifically as it relates to guideline directed therapy, um it's A to B recommendation for re revascularization, that's largely reflective of the fact that it's difficult to collect data and derive definitive treatment algorithms um in this population. So the largest trial we have is the decision CTO trial. This is a prospective open label randomized trial eligible patients included those with silent ischemia, stable angina or A CS. So a pretty broad population, but a lot of those a disproportionate number fit into the first category of silent ischemia. So not all of these patients were symptomatic, they were randomized to receive either PC I or no PC I for qualifying CTO lesions. All patients were vascularized with respect to any non CTO significant lesions. Um and the target sample for this to derive uh clinically meaningful outcome or, or I should say assess the end points of interest in uh in appropriately powered fashion was 1284 patients, but it was terminated early due to slow enrollment. Importantly, in this patient population, all patients were randomized before revascularization of their non CTO PC I lesion. So we don't know if they were symptomatic with respect to their CTO PC I. In addition to that, we just saw that they failed to complete the enrollment as expected. And we also saw a 20% crossover. So the data from this trial is very difficult to interpret, but it was functionally equivocal in the intention to treat uh population where we didn't see any demonstrable difference in functionally a mace end point. But if you look at the as treated population, there was a a compelling trend towards statistical significance. Although the P value didn't quite reach significance but certainly hypothesis generating. And the other trial that I think we have, that's, that's large enough to help guide therapy done in a more contemporary fashion as it relates to how we generally approach these patients in clinical practice is the Euro O CTO trial. So this again, prospective multi center randomized trials, these patients were symptomatic with at least one CTO and randomization occurred after revascularization of any non CTO lesion. So these patients had to be symptomatic and they had to be symptomatic with respect to their chronic total occlusion. And the primary end point here was quality of life as assessed by the Seattle a questionnaire. And um we did see a considerable improvement in quality of life both related to frequency of angina physical limitations and overall quality as assessed by this metric um in this population. Now, I think importantly, what we're really interested in evaluating when we look at the, you know, clinical trials for this population is whether or not restoration of myocardial perfusion is associated with improved outcomes. So we know that we have ischemia in these uh areas subtended by CTO if we improve perfusion to this area with successful revascularization and good revascularization, are we expecting to see an outcome? And so this trial looked at that in 212 patients where they assessed quantitative pet perfusion imaging both before and after and correlated that with hard clinical outcomes. They looked at uh perfusion uh differences uh and increase in hyperemic myocardial blood flow both before and after and it turns out that patients with extensive ischemic burden reduction and no residual ischemia as conclusively defined by pet after their PC I showed a considerable long term benefit with respect to hard end points including all cause death and non-fatal M I. So, um there's compelling evidence to suggest that in appropriate selected patients, we get, you know, good uh clinical outcomes in patients, uh you know, and revacation of CTO lesions. So the theoretical benefits certainly uh improve symptoms, which I think we have fairly compelling data to suggest is is a is a hard outcome. Improve marial function, prevent arrhythmias and improve tolerance of future coronary events and shock. Uh and and by extension, improve survival. Contemporary techniques have uh you know, they've evolved significantly in an experienced operators hands, success rates up to 90% have been achieved. Um success rates in the general population. All comers across all centers are a little bit more variable and range from about 60% to almost uh 90% again. But there's some risk to doing this average risk here is about 3% of serious adverse events which is higher than in your general conventional PC I categories. So what are we looking at when we see patients come in? Certainly, in addition to clinical characteristics, generally being symptomatic CTO coronary disease, we spend a great deal of time reviewing the angiogram. So, you know, certainly you look at a an angio and you can see whether or not a vessel is included in a matter of seconds and sometimes if there's complicated anatomy, it takes a minute. But we look these angiograms 10, 15 minutes where we're just staring at the lesion trying to understand the proximal cat morphology, the distal cat morphology the lesion length, the composition and course uh the distal vessel health and the collateral circulation, which serves as both an avenue for perfusion to maintain viability in the sub tended myocardium, but also as an avenue for visualization. So we can see beyond the chronic total inclusion. Uh while we're intervening and potentially delivery of our equipment to open the vessel, we use a variety of risk scores uh based on evidence that's been collected throughout the CTO trials to help define whether or not we're likely to be successful. We look at uh proximal cap ambiguity, whether or not there's a side branch at the proximal cap in the distal cap. How the angulation might affect our uh approach to intervention, whether or not an intervention has been tried before heavy calcification, all these things factor into, you know, calculable risk models that we can use to help guide whether or not a patient might be a candidate and what technique might be appropriate, which then leads to our calculation of whether or not the risk benefit ratio is of uh you know, favorable profile to suggest we should proceed. So we looked at uh you know, patient age CTO length, whether or not we need to go retrograde, which I'll talk about in a second, all as markers of potential risk of doing the intervention. And that's an important calculation and guiding patient therapy. So how do we approach these PC is from a procedural standpoint and what makes them different from our conventional PC I. So, um when we look at a blockage, we have multiple ways we can address this. We can go antegrade through the blockage. That's, that's most akin to what we do when we're addressing, you know, kind of your run of the mill. Um And ST Emi uh and we can go retrograde through the blockage, which is unique to CTO PC I where we might come through a collateral channel uh and come back where, but if we can't get through it either forward or backward, then we have the option of potentially going around it via the subintimal space, the layers of the vessel going around the blockage inside the vessel and then returning to the true lumen on the distal end to uh achieve revascularization. And each of these approaches has its own unique profile of uh risks and benefits and certainly um needs to be considered when you're counseling a patient through the uh benefits of, of reasor organization. So I'm not going to go through in detail all of the uh intricacies of this plot. But basically, we approach product total inclusions with a, an intent or what we think is likely to be the most viable approach to this technically but stay fluid and make sure that we're pivoting if something's not working. And so we have to kind of have plan B and C in mind so that we can make sure we're not just kind of radiating somebody without making much progress and so on to some, some cases that I think are illustrative. So uh the first case, I'm gonna show an antegrade wire escalation. This is kind of similar to conventional PC I, it's a 55 year old gentleman with refractory Angina and heart failure. Um He had an ef of 25%. So this is his diagnostic angiography has uh totally included L ad at the ostium nearly flush. Here, you can see in this caudal projection. And then on the other side, we have the right coronary artery that provides collaterals to the uh to the left anterior descending that we're interested in. Now, I think there's uh some common thought that since the vessel has been chronically occluded, that attempting to intervene is unlikely to cause any, you know, specific problem hemodynamically. But we have to really be mindful of the fact that collateral circulation is often keeping the patient hemodynamically stable. And if we're to interrupt any of that, that we, we can see hemo anemic compromise and that often happens in CTO S um particularly in, in patients that have uh specific uh features that might prone them to hemodynamic compromise, similar to any complex BC I. In this case, we're operating on the, the left main um with, with reasonable collateral to led. So we elected to place an impala and here we're using dual injection angiography. So we have two catheters in rather than one here, we have the retrograde showing us the pacification of the distal led. And then we give an Antegrade injection. We can see that the, the inclusion is, is rather sure there's some calcification there. Um But, but we have AAA beak there kind of at the proximal cap that's likely to allow us an antegrade channel. Um So here we have a wire in our uh distal vessel. Um I can't really see that well. Uh But you can see on the left side, we're probably not true. Lumen, we redirected our wire on the right side to achieve a true. And we're using slightly more aggressive wires to do these oftentimes than we might and something like a semi with stiffer tips and tapered tips or more lubricious tips that can ultimately um cross channels that might not be accessible with something like a run through wire. Notice that we're using retrograde injections to confirm our position distally. Once we cross the lesion, if we've gone subintimal, if we inject Antegrade, we are prone to creating a dissection in the vessel and a Hema uh a hematoma within the subintimal space that can make it difficult to either successfully revascularize and potentially disrupt the architecture distally and, and actually cause harm. So we're relying on our retrograde injection um to see that we have our wire in a good Truman position and we're advancing a micro catheter across that. And now we're completing our intervention in a more conventional fashion. Once we've confirmed that we are where we want to be, we have kissing balloons here on the left to maintain patency of the diagonal side branch and then proximal optimization in the left main, which will be talked about a little more later, but it's pivotal, the good left main intervention. And here we can see restoration of flow into the uh into the L AD here. Uh You'll note uh a lesion in the circ we did ifr that and it was negative. So we elected not to fix it. So now is a case of retrograde, which is, is certainly different than what we often encounter when we're doing our conventional interventions and patients uh who come to the lab, this 56 year old gentleman with coronary disease, he had cabbage and progressive refractory, an you know, he's had bypass before and here is diagnostic angiography shows a total inclusion of the circ which is basically flush. He has a patent Lima, but he has good size diagonal branches that we want to preserve. And he has um a vein graft that goes to kind of the proximal branch of a bifurcating om, but that om is now quite disease. So the vein graft while you know, letting us visualize the vessel distally is not providing enough flow to uh prevent recurrent angina. So in this case, we have a dual injection that shows a rather short lesion, the distal caps at a bifurcation of the avery groove circ and the, the om branch, the proximal cap is nearly flush and blunt. We tried with limited um you know, attempts to achieve antegrade uh wire uh entry into the distal tree lumen but weren't successful and we don't want to lose the side branch here. Uh or in this case, the led. So on the left here, um I don't know if you can appreciate this, but we've wired through the vein graft, retrograde or backward into the guide catheter and into the micro catheter that's in the antegrade space, which is now going forward. You can see that over the um initial wire past the anastomosis of the vein graft into the um true lumen of the distal vessel. We've confirmed that with a retrograde injection that were micro catheters uh across the totally occluded segment. And we've redirected our wire now um and stented according to what's common practice and restored flow. So now we have good perfusion to the lateral wall and we've managed to do that without doing a complex vein graft intervention which we know has a high likelihood of uh reocclusion at a later date. So hopefully, this is going to be a more durable approach uh to this particular situation and then finally retrograde via septal perforating branches, which is commonly done in CTO PC I. We have a 72 year old man with a refractory angina stress test consistent with inferior ischemia and he went on uh diagnostic angiography, we have uh a functional total inclusion of the RC A that's really a collateral uh bridging collateral of, of the right, you know, looking at it, we thought we might have an antegrade approach here. Um But we certainly see good septic collaterals that allow us some opportunity to, to uh to revascularize via a retrograde approach if we're unable to get antegrade. And so, in this case, we have our, our uh dual injection angiography again, a rather short occlusion with a reasonably healthy distal vessel which is quite large, good septal perforating collaterals here from the donor led, we tried to get antegrade. Um Here, we can see that I'm in a distal side branch. So really uh not having much success here and, and passing a wire as we would through a, a general inclusion. Um Here, I'm trying to parallel wires. So I know that my uh initial wire is uh is in a sub pha or a side branch and trying to get an integrated wire. And I've elected to go retrograde. So we can see on the left side um also a wire that's gone through a septal perforating branch into the uh uh RC A and, and we were unable to get the wire to go from the true lumen to the true lumen. So what we've basically done is enter the subintimal space from both an Antegrade approach and a retrograde approach. And so we're kind of making sure that these two wires meet up. We're then creating some fenestrations with a balloon and wiring retrograde. So now we have a wire externalized from one catheter into the other. So one wire that's going across the cardiovascular circulation coming out to the other end and again, completing our intervention in a conventional fashion where uh we're now able to restore perfusion distantly. So these are patients that 10 years ago, we probably wouldn't have been able to treat. We've, you know, learned from a lot of our colleagues that are probably, you know, innovating at a faster pace than, than most of us and, and devised these techniques and we've adopted them and work with them to um kind of provide this care to, to our patients. And it seems to be conventional to show a picture of your family after one of these talks. So I decided to uh incorporate that today. So this is uh my wife and Children and somehow that equates to thank you to your attention. Published October 17, 2023 Created by Related Presenters Paul Lavigne, M.D. Sentara Cardiology Specialists View full profile
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