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EP Fellows Curriculum: AF Ablation - The Non-Pulmo ...
EP Fellows Curriculum: AF Ablation - The Non-Pulmo ...
EP Fellows Curriculum: AF Ablation - The Non-Pulmonary Vein Trigger Ablation Approach
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Thank you, Nishant. I hope you can hear me well. Thank you for the opportunity. I will try to, you know, my slides and presentation have been done several times, but today I will focus on education and fellow, so we'll go slowly and try to let you understand the concept behind this. So the non-PV trigger approach, and these are my disclosures here that are always important to be displayed. So why we developed a non-PV trigger approach? All of you may think that everything comes from the treatment of persistent atrial fibrillation, but you will see that the non-PV trigger approach applies to everything that is a non-PV responder. But the most misleading article for our approach is this paper that you all know, the STAR-AF2 on New England General Medicine that compares inpatient with persistent atrial fibrillation on PVI, PVI plus lines, and PVI plus CAFE. And this paper showed that PVI only is as good as PVI plus line, PVI plus CAFE. But this is what the interpretation of the media was. This paper, in my view, is PVI only is as bad as PVI plus CAFE and PVI plus electrograms, plus lines. Because if you look at 59%, this is on medication. If you look into the paper and you go off medication, success rate of all of these three groups goes down and the lowest success rate is 40%. So in my view, 40% is not success, is actually a way not to do ablation. And number two means that PVI does not work as well as PVI plus line, PVI plus CAFE. And this paper does not go against our non-PV trigger approach because they did not went after triggers, they went to CAFE and lines. All I know is that in this paper I published in 2009, is that inpatient with paroxysmal atrial fibrillation, you can see that PVI only is much better at one year off drugs than CAFE only, 12% in paroxysmal, and there is no difference between PVI plus CAFE and PVI only. This show that PVI only, it's okay, it's good, works very well off drugs in 75% of the people, but where are the remaining 25%? Why 25% of these people are not having success? Majority of people will say because of a PVA reconnection, but over time with high power, short duration, with a lot of new techniques, everybody has encountered patient with paroxysmal atrial fibrillation and silent veins with recurrent AF. So we know that this 25% is not PVA reconnection, but it is something else and we need to focus our attention to that. So many ways have been described to isolate the pulmonary vein from osteal to wide antral to PVI plus posterior wall, and this is a technique that I learned from my mentor, and the idea that we do have is that long-standing persistent atrial fibrillation is like a metastatic cancer. When you have paroxysmal atrial fibrillation, you have cancer that is localized to the primary source, and if you don't intervene, the primary source reduces the relevance and more areas need to be burned outside of the pulmonary vein as a cancer spread outside of the primary source. And this concept is important and actually has been now kind of demonstrated by, for example, the EAST-AF trial recently, the ESC, early ablation better outcome than late ablation. Why? Because you are intervening in an early stage, like you intervene early in a cancer stage. The earlier you intervene, the better is the outcome. And this slide, many of you may have seen, many not, but I will explain to you. So my idea or our idea is that when you have paroxysmal atrial fibrillation, the majority of the trigger are in the pulmonary vein, but not all of them. And these are the so-called non-PVI responder patients. When the AF progress from paroxysmal to long-standing persistent atrial fibrillation, the relevance of the PVA triggers goes down. You can see here, and the majority of the trigger are localized outside of the pulmonary vein. This is why if you have a persistent patient or a long-standing persistent patient, if you only isolate the pulmonary vein, the chances that that patient will stay in sinus are very, very small. So we develop the so-called non-PV trigger approach, which includes the isolation of the pulmonary vein, of the superior vena cava, of the lapital appendage, of the carotid sinus, in many cases, the ligamental muscle, and the posterior wall, and others like the septum. We already kind of know the pulmonary vein. I'm not spending time on pulmonary vein isolation. We know that high power, short duration, or new technology to do that, it's good, and we need to do that. But we always isolate the posterior wall. And why? Because the posterior wall has the same embryologic origin of the pulmonary vein. And so if you believe pulmonary vein are arythmogenic, we do believe that the posterior wall is arythmogenic. And how we do that, we move the circular mapping carotid around all the area of the posterior wall until we achieve complete electrical silence of the posterior wall. This is not easy to be done. And to say if it works or not needs to be done properly. Really, it needs to be done properly. Really properly. Then we go after non-PB triggers that we try to induce. And what we do, we use isoproteranol challenge test, starting from beginning at a high dose, and not after a few minutes, from beginning at high dose for 10 to 15 minutes. It's important to say that we always place the carotid in this way, with a duodecacarotid from the internal jugular, always a double transeptal. We place the circular mapping carotid in the previously isolated left superior pulmonary vein, and the ablation carotid in the previously isolated right superior pulmonary vein. And this is my mapping system. I don't need anything else. And I start isoproteranol testing. You can see here after three minutes of isoproteranol testing, you have a tachycardia. And if you go with your mouse, this is sinus rhythm V, this is coronary sinus, and this is the circular mapping carotid. I want to clarify that CS1-2 is a distal CS, and crista-910 is high rate yttrium at the level of the SVC. So if you go here, sinus, tachycardia looks, let's look for the earliest activation, it looks it's coronary sinus 910, but actually it's crista-910. Crista-910 is at this level. So most likely this is an SVC tachycardia. To help you understanding what we do, I put colors here. So in this blue, you have the coronary sinus. In yellow, you have the vein and the far-feed left fetal appendage, since the vein has been isolated. In magenta here, in pink, you have the right superior PV. And in green, you have the right yttrium. And the 910 here is the SVC area. And you can see here, this is the same one as before. This is a green tachycardia starting from crista-910. So this mapping system allows me to know this area is triggering this AFib tachycardia. Therefore, this patient has a trigger that is outside of the pulmonary vein. And similarly, you can see this one is a coronary sinus tachycardia. You can see that the earliest activation comes here, sinus, sinus, and during isoproterinol, you have this tachycardia starting here. And the color helps you understand how we do that. And this is a PAC, for example, clearly coming from the far-field left fetal appendage. And we will say that PAC are as relevant as the sustained arrhythmias. So I would like to say that why PAC is important? Well, we demonstrate in an abstract only, not yet in a paper, that PAC are as important as sustained and non-sustained tachycardia because patients are usually under general anesthesia, and this suppress a lot of non-PB trigger, a lot of sustained arrhythmias. So we run this study where during isoproterol test, we only had PAC from some of these non-PB trigger area, and we ignored them because the physician said they are non-clinical and look at the outcome. Then we have a group of patients that actually went after these non-PB triggers initiated by PAC, and they were ablated. And you can see that the outcome is very similar to the non-PB trigger where there was no PAC, but there was the reinitiation of IAF or other supraventricular tachycardia. You can see the success rate similar, but of course the best success rate was in the patient and during the isoproterol test had no PB triggers, no PAC, no non-sustained arrhythmias during the test. And this is the distribution here of the non-PB triggers, and the coronary sinus is the one that has the highest impact. Over time, we try to think and analyze the data and understand, okay, the non-PB trigger approach works very well for persistent, long-standing persistent, which are the paroxysmal patients that we should include. And this is a table that summarizes the group of people where we know that it doesn't matter if they are paroxysmal, persistent, long-standing persistent. It does not matter. We know that this patient, older age, obesity, sleep apnea, CV scarring, hypertrophic cardiomyopathy, mechanical valve, late recurrence, post-PBI, this patient have a natal fibrillation that do not originate from the pulmonary vein and you need to do something else. So the superior vena cava we showed in this old paper at the Cleveland Clinic that looks promising as an adjunctive strategy to pulmonary vein isolation and should have been considered in a bigger trial. How we do that? We advance the circular mapping character fluoroscopically or without fluoro with 3D mapping to the area of the SVC. We always use intracardiac echo to locate the junction between the right atrium and the SVC and this is where we start, we burn and we isolate the superior vena cava. And this is another example of a firing from the SVC. Again, it's important that you play with your intracardiac echo to locate very well the area of the junction. This is the right superior PV, so you need to be a little bit higher at the junction, almost at the level of the pulmonary artery, right above you have the SVC. And we show that empirical ablation of the superior vena cava, even in paroxysmal patients, play an important role. The coronary sinus is another area where we like to put a lot of emphasis and focus. And how we burn or isolate the coronary sinus? Well, we do it endocardially because we have two kind of transeptally and we go all over the coronary sinus and epicardially, going from the right side in the coronary sinus. And we move this catheter up and down, up and down frequently in order to achieve isolation. This is an example here of tachycardia coming from the coronary sinus. I showed you before one. And there is a paper that showed that, can you do focal ablation? Well, the focal ablation does not work as well as the isolation of the CS. And so we believe that you should not just do the focus, like CS3-4 is the earliest you go there, but the whole coronary sinus should be isolated. And these are other example of coronary sinus tachycardia here. Other example, other example here. And this is an example of PAC. Look, consistent PAC from the coronary sinus here. And another example here. So this is again, a tachycardia coming from the coronary sinus. We are burning here in the coronary sinus to achieve CS isolation. You can see CS1-2 is flat. CS3-4 is flat. And we are here at the level of 5-6 trying to isolate. And what we mean by isolation? Look at this. This is a clear signal that we want to eliminate. You can see here the signal of the coronary sinus is eliminated. The double component is eliminated. And we actually have dissociative firing from coronary sinus. This is what we believe or we think when we talk about coronary sinus isolation. Another controversial non-pivotal area that is present in the literature is the left fetal appendage. And I know many of you here at the institution to isolate or not isolate the left fetal appendage and how dangerous it is because this isolation might be pro-arrhythmic and pro- thrombotic. Sorry, I said pro-arrhythmic. I meant to say pro-thrombotic. So there is histopathologic evidence of automaticity cell into the left fetal appendage that's demonstrated here. And in 2010, meaning 10 years ago, meaning we started this in 2008-07 because this paper was published in that. So we go about 15 years ago. This is the first paper on circulation where out of 4,000 patients, 987 came to our institution for recurrent atrial fibrillation for redo, two, three procedures done. You can see that 29% were paroxysmal. The majority were not paroxysmal. Well, we shocked this patient and we put them on isoproterol. And we found that in 73% there was no left fetal appendage firing, but 27% had a left fetal appendage firing, including the PAC of the presence of PAC in the definition. I want to emphasize that. Not atrial fibrillation firing, but PAC firing was part of this 27%. And you can see that 18% were paroxysmal, meaning these people with two, three ablation, they were still in AFib with demonstrated isolated veins. All of these 987 patients had demonstrated isolated veins. And I'm sure in your institution, you have patients that come back, you put the catheter in and the veins are isolated, but the patient are in AFib. And you can see that the appendage was ignored, focally ablated, or electrically isolated. And you can see here that ignoring the appendage give you a success rate of less than 20%. Focal ablation was actually very bad, like not doing anything for the outcome. And the best way to achieve a high success rate, extremely significant from here, was the complete left fetal appendage electrical isolation. How we do that? We do that by putting the circular mapping catheter at the ostium of the left fetal appendage, and we isolate the appendage this way. And this shows you what we mean by isolation. You can see the double component of the appendage here and the left fetal appendage electrical isolation. This is not easy. You can see here how thick is the appendage. There is risk of perforation when you do that. But with a good learning curve, this can be learned. Differently is when you try to do lines, we discourage to achieve appendage isolation with lines. We believe this way of doing it is more pro-arrhythmic. In this paper though, they show very well that the learning curve is pretty good. You don't need many cases. And the complication rate with tamponade goes down to only 3% after only a few cases of a learning curve for appendage isolation. So I think that it's important to say that you need to buy the price of a learning curve, but you can achieve that. Now, we were saying we don't do trigger ablation for paroxysmal AFib. We empirically do the vein. Why in patients with long-standing persistent ablation where the success rate of PV only is low, why we have to see a firing? Why cannot we do an empirical left fetal appendage isolation? And we designed a belief trial where 173 patients were randomized to an extensive ablation plus the empirical ablation of the appendage, no need of firing versus no appendage. And that's the outcome. This is the postulal wall, the graphic design from Jack. You can see that both groups are the same with the difference that here the appendage is isolated and here the appendage is not isolated. But both groups have veins, postulal wall, coronary sinus, and SVC ablation. This is the outcome. You can see that after two procedures, or 1.3 average procedures, in the people doing the appendage, the success rate was 76% in long-standing persistent patients. And the success rate of the other group that had the appendage done only after the second procedure was 56%. And I think this paper was pretty good to show the relevance of that. Were we the only one doing this? Well, over time from Bordeaux, from case report, from the use of the Lariat registry, many have shown the relevance of the appendage to achieve sinus rhythm maintenance and follow-up. Some people start doing this with the cryo balloon, which is also good to achieve left-fetal appendage electrical isolation. And with Dr. Romero, my former fellow, now my attending here in Montefiore, we put together and made analysis because there were eight, 10 papers showing left-fetal appendage isolation data. And you can see that all type of recurrence favors the left-fetal appendage electrical isolation, as well as the stroke risk is not increased in this group. Importantly, in this table, we have that if you look at how much RF time you have to add to achieve isolation, these three groups that don't talk to each other have the same numbers. About 20-25% RF time extra to your ablation needs to be added to achieve electrical isolation. And we concluded that regardless of the method and technique used, left-fetal appendage electrical isolation, in addition to start-down ablation, appears to have dramatic incremental benefits to the freedom from atrial fibrillation and follow-up. There is this other meta-analysis of Jackie P that reproduced the same and added actually surgical technique with the atrial clip to achieve isolation. And the field is expanding in this area also with surgical or minima in basic surgical techniques. We have also published a paper on how we achieve left-fetal appendage isolation with fluoroscopy and without fluoroscopy by putting attention on the identification of the phrenic nerve and the left main if you want to do it fluoroless. And this can be done with fluoro or without fluoro in the same way. The field is expanding and many more papers are showing basically the same. This is another paper showing the technique of surgical and endocardial isolation of the left-fetal appendage at the point that in this editorial we push the field saying should we change in our practice for the ablation of persistent and long-standing persistent atrial fibrillation, we need bigger randomized controlled trials to do that. The field is expanding because also the Lariat people now purchased by ATRICUDE designed the AMAZE trial where the patient will be randomized to Lariat procedure with the position of the Lariat that I guess all of you know how it works. And, you know, it tied the appendage achieving mechanical electrical isolation and patient are randomized to PBI only versus Lariat followed by PBI. And this is a randomized control trial that with a two to one randomization has enrolled 600 patients, 400 patient Lariat PBI, 200 patient PBI only. The study is closed for enrollment. I guess in 2021 HRS meeting, we will have the results and I'm very curious about them. The only limitation of the trial is that posterior wall coronary sinus were not part of the ablation setup. And I think this area add some success to the appendage and we'll see what the outcome is. I will jump this slide for the sequence of time. I just want to show you that even in patient that put the clip, you might have a stump of the left fetal appendage and this stump is very arrhythmogenic. This patient did four ablation and had this tachycardia coming from this area from the stump of the left fetal appendage. So even if the appendage is closed surgically, that area has an electrical activity that has important relevance. And I want all of you to keep this in mind. Something that we recently published is a unusual pattern of isolation of the left fetal appendage where by doing endocardial CS ablation here, you can see by mapping the appendage, the lasso is in the appendage, we achieve isolation of the left fetal appendage. You can see here. And here by doing a epicardial ablation, again, the mapping color that is in the appendage, we achieve isolation of the left fetal appendage with coronary sinus ablation. We had many of these cases and we start prospectively collecting these cases. And what we found is that by shooting contrast, when we were involved in the ligament of Marshall protocols, we found this vein here that connect the coronary sinus to the left fetal appendage. Well, this vein has been considered the ligament of Marshall, but the CT scan clearly showed that this is not the vein of Marshall because this is the vein of Marshall and this is a different vein. Secondly, this is an anterior vein, as you can see here from the CT scan and not a posterior vein as the ligament of Marshall or vein of Marshall. Therefore, we have called this the Aldeban vein from my name and the one of my mentor, Dr. Natale. And that has been also described by Dr. Cabrera histologically here as an additional left fetal appendage coronary sinus vein connection. So I think there's something here that we really need to learn and expand in our understanding of the vein connection. And that's why the non-PV trigger thoracic vein approach work. As a non-PV trigger, the vein of Marshall has a history in showing its arrhythmogenicity that goes very far away in 72. And, you know, the work of this has been then reproduced recently by many authors and more recently by Dr. Valderrabano that in canine model and in human model have shown how the ligament of Marshall is very important. This is the first human experience of alcohol ablation of the vein of Marshall. And he achieved, you can see here an induction of AF from the vein of Marshall with high frequency stimulation and he achieved success. And he has designed the Venus and Mars trial which was an NIH trials. The results were presented in this ACC late breaking trial. And we still don't have the full manuscript out but very interesting data. Now what's the thrombogenic risk of left fetal appendage isolation? Well, can you stop anticoagulation? What's happening there? So when we start doing this in our 2010 and 16 paper we were looking at these three parameters mitaling flow, left fetal appendage, flow velocity, contractility. And we found that if only one or the other were there this was happened in 50% of the patient as shown here. We learned over time that you don't need each of them to be abnormal to consider the flow velocity abdominal one of them abnormal is equivalent of abnormal. And so this 50% is now in the settings of 80%. Meaning if you isolate the appendage the flow velocity of the contractility appendages impaired in 75, 80% of the patients. But in some patient, this is not the truth. This is a pre and post flow inpatient that had an appendage isolation. And this is important. You show here that the flow velocity is about 0.2. This patient cannot stop anticoagulation otherwise they will have a stroke or a TIA. But different data have been shown in Germany with a high degree of clot and stroke inpatient that underwent left fetal appendage electrical isolation. But the difference is in their lesion set. They have done a lot of lines as shown in this slide before. And I think that isolating the appendage this way create a lot of problem with the atrial contractility. And I think this way is more prone to formation of clot than our technique. Another misleading paper that said if you isolate the appendage even if you are on anticoagulation your stroke risk is high. And they see this paper here but you can see that the patient post ablation were not on anticoagulation. You get this paper. This patient was on clopidogrel. This patient was on clopidogrel. This patient was on no anticoagulation. Two people were on cubadin without documentation of the INR level. So these people had a stroke because post appendage isolation they were not on proper oral anticoagulant. And we are stressing out that after an appendage isolation you need to be on compliant oral anticoagulation. The field of appendage isolation is expanding. Many people are reporting that and they are saying that with PV only AFib is back. There's nothing you can do about. Another misleading information is the interpretation of the TEE that we do to understand if the left fetal appendage is impaired. We have some cases where the patient are in sinus they do the TEE and we are told, oh maybe there's a reconnection because the flow velocity is normal. But this is not normal because look at the contractility of the appendage in this video. And you can see that the PR interval is the one where the flow velocity needs to be calculated not the flat line here. So this patient does not have 0.7 this patient has a 0.2 flow velocity. So this patient cannot stop oral anticoagulation otherwise we'll have a TIA stroke. So I want to show you that in this patient this is a patient in AFib that never had an appendage isolation. And this is a patient in sinus rhythm that had an appendage isolation. Yes, there is no contractility of the appendage in both but I want to emphasize the fact that the contractility of the appendage is not impaired only by the ablation can be impaired also in sinus rhythm or in AFib. And it's important for you to know that this patient basically is worse than this patient. Also, there is a passive contraction of the appendage. You can see here how there is a passive contraction of the left fetal appendage. So there is a possibility that you have some contractility even passively, but to give you data together we have analyzed more than 108,000 patients that follow a left fetal appendage electrical isolation. And we had no stroke when people were off anticoagulation if they had a normal EF or a normal left fetal appendage function. If the left fetal appendage function was impaired it was zero if they stop anticoagulation. It was 16.7% if they stop anticoagulation and it was 2%, 1.7% if they had some optimal anticoagulation, missed doses, subtherapeutic INA. So after appendage isolation, if your flow velocity is normal, you don't risk a stroke even if you are off anticoagulation but if it is impaired, if you stop anticoagulation you have a high stroke risk. If you are properly anticoagulated you are safe but if you miss doses and you're not compliant you have a 2% risk. And this is a summary. And of course, if you close the appendage which is something we recommend you don't need to be on anticoagulation and we were able to discontinue oral anticoagulation in 98% of the patients. In this paper, the authors try to close the appendage at the same procedure of the ablation and this is what we are talking here but I cannot discourage that because there is a lot of edema that forms and so you may miss the good sides of the closure if you do it the same procedure. So I think, look at the edema resolution and the gap that this patient have. So I would say that if you will plan for closure plan it at follow up three to six months post ablation. Can pulse field ablation be the solution? I'm trying to work with Medtronic on something like that. This is a porcine model where I try to do a right at appendage isolation with the pulse field ablation. It looks very promising, looks good. Of course I have no clinical data but all the information I gave you they need a bigger randomized trial and we have designed this plea AF trial that is open for enrollment where all patients with persistent lepidopersistent, long-standing persistent atrial fibrillation with a child mask of one or higher will be randomized to PVI alone, PVI plus posterior wall, PVI plus posterior wall and left at appendage isolation, PVI plus posterior wall, left at appendage isolation and coronary sinus ablation. And in case of recurrence, the operator is supposed to redo the same lesion set of the first ablation if any reconnection of the prior lesion set was there. So this paper or this protocol will give a lot of answer on what is the real success rate of PVI only? What is the real success rate of PVI and posterior wall? What is the real success rate of PVI, posterior wall and appendage isolation? What is the real success rate of PVI, posterior wall, appendage isolation and coronary sinus ablation? About 233 patients per group will be enrolled with a total of about 1000 patient, about 900 and something. So I'm excited that this trial will give us a lot of answer and we'll probably give also a lot of information about all the data that I presented during this talk. So I would like to conclude that left at appendage electrical isolation appears the most relevant target to achieve freedom from arrhythmias, especially in patient with non-paroxysmal retabulation with documented sided PVs and following ablation of other relevant triggers such as coronary sinus and posterior wall that stroke and TIA following left at appendage electrical isolation may occur regardless of the child birth score and mostly when patient are off oral anticoagulation, non-compliant oral anticoagulation or under the care of unaware physician that they decide their oral anticoagulation discontinuation. Left at appendage electrical isolation should be considered risk factor for stroke TIA and indication for LA closure device or lifelong oral anticoagulation should be considered irrespective of the child birth score. Bottom line, sinus rhythm should be the rhythm of all electrophysiologists, all of us and for me is the only music that I like to hear in the EP lab. Thank you very much for your attention. All right, that was great. Thanks so much. Just a couple of questions here, maybe if I could ask you. One, there's a couple about isopril, you know, the protocol. So if you're mapping PACs and you're giving high dose isopril, how do you distinguish between catheter induced PACs versus an actual trigger? That's a very important question. The first thing is that we go on iso and we go on fluoro and we see if the catheter are kind of inducing PAC, first of all. So second, we have a very stable catheter here from the IJ. This catheter is super stable. That's why we don't recommend the groin because from the groin, it's not very stable. Second, we don't put this catheter into the left fetal appendage. We put this catheter in the previously isolated left superior PV. And sorry, in the previously isolated left superior PV. So if you have a far field PAC from the left fetal appendage, it's less likely that this is inducing it because this is in the vein, it's not in the appendage. The same here, this catheter here is in the previous isolated veins. And if you have a far field PAC, it's clearly from the superior vena cava and not from the vein, which is demonstrated isolated. The issue is sometimes if the catheter is moved a little back from the coronary sinus, that can be the case. But usually we can differentiate catheter induced PAC from really PAC. And then there's a question about how much significant hypotension do you see with high dose isopril under general anesthesia? Very good. This is extremely important. Actually, I spent almost a year to complete the education of the whole anesthesia team here because they change all the time. People come down, new fellow, new resident, new CRNA, new doctor. Every time it's a new... So I had to give three grand round to achieve that. Before we start the isoproteranol test, titration with phenylephrine from anesthesia has to start. They need to start giving phenylephrine before you start and then titrate with the increased rate of the response to the isoproteranol. And if you do that, you never encounter or very rarely encounter low blood pressure. It's important to say that we differentiate our protocol from the UPenn protocol, where they started two mics, two minutes later, they go four mics, two minutes later, they go six mics, two minutes later, they go eight mics. I think that you don't have enough time at high dose. So what we do, we start at 20 mics from minute one and you need 10 minutes of 20 mics to really see something in the majority of the time. And don't forget that you wait another 10 minutes during the washout. Tachycardia or PAC during washout are as relevant as during the initial 10 minutes. So both part are very important. Now, people that wanna go fast and don't spend time, well, this adds 25, 30 minutes to the procedure time because 10 minutes to start and 10 minutes to wait, it's another 20 minutes, but it has one advantage. It allow me and force me to wait 20, 25 minutes and to recheck my veins, which usually you recheck, you get out. I always recheck my vein after these 20 minutes and with the work of the ISO that can work as adenosine to give you reconnection and force me to wait, I end up when necessary to retouching the vein and making sure that the possibility of PB reconnection and follow-up goes down. Okay, and for SVC isolation, how do you overcome the phrenic? So the majority of the time you can isolate the SVC by staying septal or posterior septal, even if, because you don't need, as for the vein, you don't need a full pass to achieve isolation. And I can tell you that if you work posteriorly and septally, you can isolate a lot of SVC. Once the area that really needs to be burned is on the phrenic nerve side, of course you map the phrenic nerve and you create a phrenic nerve map. And then I have a duodecacharacter here, so that's why I recommend to do this. We can pace and we burn while pacing as we do for cryo. And you stay as posterior and below the phrenic nerve area. So from the anterior part, you go posterior to the area that is there. And from far away, we published this in a Heart Rhythm Journal paper, you can isolate the appendage. Why constantly pacing? If you cannot do that, you go as close to the phrenic nerve while pacing and you try to isolate the SVC. It's very rare you cannot do it. Probably it's 1-2% the amount of patient that you cannot achieve it because of phrenic nerve. Now, if you are doing empirical isolation, you don't have to do that, you just quit. But if the patient come back with recurrence where you know it come from there, that the tachycardia is like an inappropriate sinus tachycardia type patient, then the only way to do this is to do an epicardial access, put the wire over there, inflate a balloon, separate the phrenic nerve from the endocardium, go back endocardially and while pacing, burn endocardially with the balloon that separate the phrenic nerve. But of course, you don't do this in an elective procedure, you do this only in the patient where you have really the necessity to isolate the SVC. All right, and then I guess, you've been doing this for over a decade now consistently. So do you have a sense that there's a consistent trigger that maybe should always be targeted, like the posterior wall, just take out the posterior wall in everyone and then look for the other triggers or is there nothing that's consistent? Very good, so our lesion set in all patients from procedure one includes, I think I have it here, sorry. Oh, what is that? Sorry, includes the posterior wall. So our lesion set is PBI, posterior wall, SVC. This is my basic paroxysmal, non-paroxysmal, all my patient, I do PBI, posterior wall and at the end of the case, SVC. Once this lesion set is achieved, I start isoproteronal test. Now, we learn over time that in paroxysmal patient, this is good for the majority of them. So I wouldn't do more procedure one, I would do more at procedure two. Although if you have a patient that is female over 75 and with sleep apnea, I know that even if paroxysmal, this is not enough. So we start empirically doing more, but I try to wait for the second procedure to do that. In persistent lungs and in persistent patient, I know that this one is not sufficient. I know I will fail. So at the beginning, we were doing the isoproteronal test. Now, we go for empirical isolation of the coronary sinus and the appendage. And I can tell you that we consistently have a higher degree of success. Of course, CS and appendage have a high rate of reconnection, 30, 35%. So we still have redo patient where we have to go back and redo the appendage or redo this, yes. But the success rate of follow-up is extremely high. So I think that coronary sinus and appendage are consistently important. Okay, great. And then my last question here, what technology do you see that you're most excited about? Well, I think that the QDOT technology that is coming out with Biosense, the FDA trial of paroxysmal was concluded. The follow-up is gonna be presented. In Europe, it's already a CE mark approved. I think the QDOT will allow more people to do high power short duration or excellent lesion formation in a very short period of time. So I'm excited that that technology will allow more people to achieve quicker, consistent and durable PV isolation. And it's the cornerstone of the procedure. So like cryo did, we will have a more uniform patient with isolated veins and we can look for after. So that is something that I really like. The second one that I think everybody's attracted is the electroporation. Electroporation looks a super promising energy source that can give lesions durability and no complication because it does not affect other the esophagus, the phrenic nerve and other important structure around the left atrium. So I'm very excited about that because that technique can be built on balloon or linear catheter or we can try to do more lesion sets. So I think that's the most exciting thing that I look forward for the future.
Video Summary
The speaker discussed the non-PV trigger approach in atrial fibrillation (AF) ablation. They explained that while the majority of AF triggers are located in the pulmonary veins (PVs), there are other triggers outside of the PVs that can contribute to AF. They highlighted the importance of targeting these non-PV triggers, particularly in patients with persistent or long-standing persistent AF. The speaker emphasized the significance of posterior wall isolation, superior vena cava isolation, coronary sinus ablation, and left atrial appendage isolation in these patients. They presented evidence from studies and their own clinical experience to support the effectiveness of these approaches. The speaker also discussed the thrombogenic risk associated with left atrial appendage isolation and the importance of proper anticoagulation. They mentioned ongoing research and clinical trials to evaluate various ablation strategies and determine the optimal approach for AF treatment. The speaker concluded by stating the importance of achieving sinus rhythm in all patients undergoing AF ablation.
Keywords
non-PV trigger approach
atrial fibrillation ablation
persistent AF
posterior wall isolation
superior vena cava isolation
coronary sinus ablation
left atrial appendage isolation
anticoagulation
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