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Bringing Adult AFIB Technology to ACHD Patients (Presenter: Joachim Hebe, MD)
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Next speaker I'd like to introduce is Joachim Hiebeck. He brings us AFLIP technology to adults with congenital heart defects. Joachim. Oh, thank you very much, Brian, for doing this for me. Good evening, ladies and gentlemen. It's a big pleasure being here. As Michael Epstein already has done the talk, which is my absolute favorite talk, but he did a good job, I was asked to talk a little bit about atrial fibrillation. Maybe it's due to the fact that 10 years ago already I promised ongoingly that we will talk in future about atrial fibrillation congenital heart disease. And I think everybody realizes that this is a topic of the future, even for the present at the moment. And in the next 10 minutes I will go through these points quickly like a fly through these points with you together. We know that our population is aging post the adult congenital heart disease population, and this is just from the German registry just as an example. Since 1995 we have more adult patients than young patients with congenital heart disease over 18 years of age. So we guess that we have over a million people in the adult population with congenital heart disease in the U.S. In Canada 100,000, Europe 1.8 million. And we know and we realize that arrhythmia is the leading impact on morbidity and mortality next to heart failure. And atrial fibrillation already 10 years ago was promised to have some impact on mortality. Morbidity has some relation to stroke, heart failure, and need for cardiac intervention. This is from the Montreal group already promised. And if we see that and we know atrial fibrillation is in the normal heart population, it's a question of aging. It's a disease of aging. So I'm exactly at this point where I should have atrial fibrillation now starting on like some friends here in the room. And if you go for our adult congenital heart disease patients, we see related to the severity of the congenital heart disease we are much younger doing this atrial fibrillation. The likelihood is related to the severeness of the congenital heart defect. And there are only a few data existing about the risk or the relative risk for atrial fibrillation. And if you go through these different groups of congenital heart defects that have been published, you can estimate an average between 5% to 20% of the patient cohort having atrial fibrillation on the long-term course, except from the Netherlands group. Maybe some antiarrhythmic agents are related to cheese. I don't know exactly, but maybe they didn't draw their focus on this arrhythmia. But anyway, we see a very broad existence of atrial fibrillation, especially on the long-term course. This is an interesting study from a Swedish group. This is from the Swedish National Registry. Only atrial fibrillation coded with ICD code. And they were looking for almost 22,000 patients with congenital heart defects over a very long period of time. And they matched it with a 10 times higher control group. And you can see that the risk for development of atrial fibrillation is 22 times higher than a normal patient population. For sure, the number, I think, still is here underestimated. 684 into 22,000 patients is around 3%. We all guess that the risk for atrial fibrillation is a little bit higher. What about mechanism? Since Michelle Hazager from the Bordeaux group has found the pulmonary vein area to be the main trigger area for the initiation of atrial fibrillation, we have a revolution in the thinking of understanding of atrial fibrillation. And all are aware of this. And this pulmonary vein, ostia, or the transition from the pulmonary vein tissue to the left atrial myocardium is giving rise because of its electrical instability. And so even extra pulmonary vein areas at this time have been identified to give rise for trigger sites. But with respect to the maintenance of the tachycardia up to 2019, we have no really definite clues how the maintenance really is working on the myocardial tissue. And there are a lot of concepts, rotors, cafes, ganglions, and they were giving rise for more science and for more interventional work. And this is maybe the transition zone between electrophysiology and electrophilosophy. And finally, it turned out, with respect to strategies that we have, for sure we have to divide in rate control and rhythm control, and the tools are named here. And if you look, just for the sake of time, if you look for a very important publication from Nasser Marouche, the CARS-LAF study, and I think most of you are aware of this, looking at patients with reduced left cardiac function, so all had a function of less than 35%, that were included in this study and were looked for an endpoint of freedom of atrial fibrillation, and there was ablation very much superior to medical therapy, whether they have rate control or rhythm control. So it is kicking out, finally, rate control and antiarrhythmic drug treatment. And we know for our patient cohort reliability side effects, and it's not attractive for an average young patient population anyway. So we are talking about rhythm control using ablation or surgery. And trigger elimination, following the concept of Michel Hazager, for sure was then the concept of pulmonary vein isolation that has been evolved within the last 15 to 20 years. And for substrate elimination, going back a little bit more, we know all the concept of Cox-Mays surgery. And in his hand, Jim Cox had 80% of conversion to sinus rhythm. It was not transferable to other centers, we know, but finally the concept worked, and that was the first step we tried to mimic with linear ablation lesions in the late 80s. And on top to these linear lesions, a lot of following of these rotors and ganglion ablations have been added. But it turned out, finally, that latest with this STARA-F trial here from the U.S., from Alan Verma, we could see that no additional concept on top to the pulmonary vein isolation could save sinus rhythm on the long-term course. So finally, pulmonary vein isolation at the moment in the adult normal heart population is the concept of choice. And we know there are some other concepts going on, but it's not proven that they really save sinus rhythm on the long-term course. So this will be future development. So a quick view to the tools. We know radiofrequency current, cooled activation is the selection for most of the ablations, and next to cryo-energy. Looking for the outcome of adult congenital heart disease population, we have published 2017. This paper included 57 patients, all different types of congenital heart disease. They have been divided into mild, moderate, and severe, according to the Bethesda Conference. And 17 of these patients had previous right atrial ablations, and 16 of these patients were natural survivors. Looking for the arrhythmia, one-third of the patient population were paroxysmal atrial fibrillation and two-thirds persistent atrial fibrillation. And more patients were after corrective surgery, so 30 patients had corrective surgery, and six patients had palliative surgery. And if you look for the mapping we have done in these patients next to the pulmonary vein isolation, you can see here in this three-dimensional reconstruction, we found in some of these patients as a result of cardiac surgery areas of scarring, and in the neighborhood of these scars, in some of the cases we found even trigger sites for the induction of atrial fibrillation. And this is the concept of what we have done in these patients. We have included several ablation attempts in these patients, up to four ablation attempts, and some of them started with PVI only, and the majority of the patients had some additional ablation concepts. Finally, we were able, with the ablations, to get out this result. This is the freedom of atrial fibrillation in relation to the time cost, to the follow-up after the first procedure, and here the blue line you can see after the repeat procedures. There's another publication recently coming out from six North American centers, a multi-center study, and you can see here again it's a mixed patient population, and just quickly going through these, it's a little bit more patients that have been included, 84 patients, and PVI alone was done in 30 of these patients, and PVI and these additional concepts that are listed here were done in the rest of the patients. It's important to mark at this point that here only patients were included with a singular ablation approach, not a repeat ablation approach. Maybe I can draw your focus here on this non-PVI triggers were found in 38 of the patients, 38 of 84 patients. So this is 45%, which is non-related to the pulmonary vein ostias and to the right atrium in 22 of the cases. I think this is a big difference to the normal heart population. If you compare the outcome after one year, this is between Bremen and the North American centers. It's not far distant, so it's about 60%, let's say, for the first course of these patients, which is certainly below the results we see in normal heart population, but it's more or less comparable. Challenges, for sure, it's the excess, and it was addressed by the previous speakers already. So vascular problems we can have with cardiac anomalies, hindered excess. I just go quickly through these points. If we have ASD closure, interventional ASD closure, typically the patient have previously the ASD closure and then afterwards we were asked to do the PVI. So it should be done in the other direction, we know, but the reality looks different, and you can see that we can bypass even big amplature devices. Typically we avoid going through the amplature device, so we try to find some remnant septal tissue where we can do the puncture. It was addressed already by Mike Epstein, doing the transseptal or transbuffer procedures in the mastadsenning patients. Even these patients do have, in rare numbers, they have atrial fibrillation, so the excess is for sure a little bit challenging. Maybe some of you have seen in the afternoon session or early afternoon session, the poster session from the Mayo Clinic, trigger site elimination in the left persistent superior carval vein. We have seen this in our cohort as well, so this is an anatomical structure which is really very important to address if we are thinking of elimination of potential trigger sites. It was published already in 2004, the first addresses were done, and extra left atrial substrates, so for maintenance or for triggering. This is from the North American study, just an example where the right superior carval vein is inserted into the superior carval vein towards the right atrium, so you need to be aware of things like this. This is another point I would like to raise here. For the maintenance of the tachycardia, we typically are focused to the left atrium. It's in our cohort not necessarily the case. If you look at this MRI, if you appreciate the huge right atrium, this is in an Epstein case, it could be similar in a classical Fontan case, and I think everybody would expect that for the maintenance, maybe the right atrium in this case is relevant. This is just for the mapping situation. The blue area is the right atrium. This is again in the right atrium, and the red catheter here is in the coronary sinus, and if you see the speed of the activation, you can see that the right atrium is driving the arrhythmia in this case, so we need to think a little bit further with respect for the maintenance of the tachycardia. Access, maybe hybrid thinking. We should take home and talk to our surgeons. Maybe interventionally we can find solutions, but maybe together with the surgeons, and there are established ways to go transatrial or transventricular with the help of the surgeon. Sorry, I go the wrong way. I hope that we understand a little bit more in the future about the maintenance for the tachycardia, not only looking for the intracardiac stigmas. We need to find these driving areas, like you can see here. This is an example from a pulmonary vein, but it can be somewhere else, and just the non-one-to-one relationship to this driving area is a little bit fooling our reconstructions. Maybe in future we can learn about, with future technology, last seconds, future technology, with a high sample rate, about the real mechanism of the tachycardia, especially if they are changing from one mechanism to the next. This was addressed already previously, looking for the substrate itself, and maybe we can learn even more. This is from the decaf study from the tissue imaging that we see potential areas for the maintenance of the tachycardia, but even in the normal heart population, so far we could not guide ablation just based on these pictures, but this is something for the future. So I think out of time reasons I stop here and conclude ablation and atrial fibrillation in this patient cohort can be done, but we have to enlarge our concepts for this complex patient cohort. Thank you very much.
Video Summary
Dr. Joachim Hiebeck discusses atrial fibrillation (AF) in adults with congenital heart defects. He explains that the number of adult patients with congenital heart disease is increasing due to an aging population, and that AF is a leading cause of morbidity and mortality in these patients. Dr. Hiebeck highlights the higher risk of AF in patients with more severe congenital heart defects. He also discusses the mechanism of AF initiation and maintenance, including the role of the pulmonary vein area. He emphasizes the importance of rhythm control, particularly through pulmonary vein isolation (PVI), and discusses the success rates of PVI in this patient population. Dr. Hiebeck also highlights challenges in performing AF ablation in patients with congenital heart defects, including vascular problems and complex anatomy. He concludes by suggesting the need for further research to improve the understanding and treatment of AF in this patient group.
Meta Tag
Lecture ID
3834
Location
Room 211
Presenter
Joachim Hebe, MD
Role
Invited Speaker
Session Date and Time
May 09, 2019 1:30 PM - 3:00 PM
Session Number
S-032
Keywords
atrial fibrillation
adults
congenital heart defects
morbidity
mortality
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