But if you want to create deep lesions, probably RF is not the way to go. What about human experiences? There are very few of them. This is one of the latest. It's just three cases, and in fact in one of them even they failed, and this was more or less the idea. So the advantage of this, the potential advantages of this technology in the ventricle is that you don't need true contact of the device, but still you need some proximity to the target area. Okay, what else apart from PFA, needle ablation is another potential thing that will come in the future. Again, there are some initial experiences. This is a basic science model with this device, and they created some lesions looking for changes in local unipolar electrodes. This is one example of one of the lesions created, so a significant large lesion, and what they found is compared to conventional RF application, the depth again was significantly increased. However, at the same time, the width and the volume of the lesions were also dramatically increased. There is also this catheter has not been really developed apart from this basic science experience, but what is apparently coming is this new device that is a device that is also using a needle, but in addition to that needle is infusing within the tissue heat saline. With this, the operator can create very large lesions like in these examples, and this has been tested in some patients with apparent good clinical efficacy. However, at the same time, there were some safety concerns. Some patients developed a stroke, and even one patient died. So still interesting initial results, but some concerns about safety. What about cryo? Cryo lesions, there are things to come, and this is one of them, ultra-low temperature cryo, and this is one of the devices that are being tested nowadays. It is a device that can be shaped in different shapes according to the target, and it can go down to close to minus 80 Celsius. There is an initial study published recently, one year ago, with apparent good results both in paroxysmal and persistent at alveolation, both acutely and at follow-up, and apart from this initial experience, there are other things to come, for example, combining cryo with other energy sources, like in this ongoing parallel study, that they are combining pulse filablation with cryo energy. Other things that maybe we'll witness in the future is SBRT, so radiotherapy. You are familiar with this technology, this has been published some years ago. We have all had some experiences, like in these cases from ours, and what is coming new is the possibility to better synchronize the delivery of this radiation beam, not only to respiration, but also to cardiac cycle, in order to have more accuracy and better results. In addition to that, there has been some preliminary data suggesting that this way of ablating tissue, it may also come with some favorable effects, like reprogramming some myocardial cells, like in this example, for example, what is shown is that in some patients, what they found is that the curious complex went a little bit narrower after the application of this therapy. So suggesting that beyond creating some issues, it may have some potential pleiotropic benefits. There are some ongoing studies, however, none of them are randomized, so it still is an area that is a little bit kind of unsecure, what is going to happen with it. And the final thing that I would like to comment is about RF, because still RF is the technology or the energy source that we are using most, and you probably all of you know that what is currently fashion is hyposolideration application. And the rationale behind it is that with hyposolideration application, you may create different ablations and you will decrease the ablation time. There has been some meta-analysis suggesting that this way of applying RF current could result in better freedom of fatal ablation at follow-up and other benefits like acute PVD reconnection and procedure duration. However, we have presented this year in the era of Congress the largest randomized trial comparing conventional versus hyposolideration. Here you see the design of our trial, it was a multicenter one, randomized, comparing conventional versus hyposolideration, and surprisingly at follow-up we found no differences between the two arms, and in addition to that, no differences in safety between the two arms. However, if you go into further detail of complications, we found a significant more embolic complication in the hyposolidation arm. In addition to that, we had a sub-study of several MRI, and we found that hyposolidation was more frequently associated with sub-ischemic stroke events. So this emphasizes that whenever you are using RF, you need to ensure that you are not overheating the tissue, and in that way there are some interesting devices that are coming, or in fact they are already in the market, this is one of them, it's the Diamond Temp, that is a catheter with a special design using a diamond array in the tip, and what is interesting of using diamond is that diamond diffuses heat much better than platinum or other materials, so it can somewhat take out from the tissue a lot of energy, especially from the most superficial layers of the wall. So this is one way to go with RF, and the other way, potential way, is to try to monitor the lesion formation during your RF application and give you an example. Here is a PT, we are ablating there, and without any notice at all, you will see in a minute this explosion that was not apparent for anyone. It was only seen in eyes, so clearly showing that probably we need to monitor our lesions in the future. So not to extend myself much longer, some take-home messages, after PFA, this is still PFA, especially mainly at short-term, and beyond PBI, there is some way to go to understand better the role of this technology for line creation or for PT ablation. There are new tools coming for cryo with ultra-low temperature cryo, or combining cryo with other energy sources. Needle ablation, there are some initial results, but there are concerns about safety, and in terms of RF hypersolidation, I think that our trials show clearly that there are some concerns about safety, and there are new catheters coming, the FEDA one, that may solve part of this problem. Nothing else, thank you very much for your attention. Thank you, José Luis. We have time for questions at the end of the presentation. Now we will move on to the next talk. I invite Dr. Ana Venancio, she's a cardiologist, electrophysiologist from Monte Sinaí Hospital in Juiz de Fora, Brazil, and she will talk about subcutaneous ICD, what is the current approach. Thank you. Good morning. I'd like to thank Dr. Ulysses Rohel for this invitation, and also Molio and Mauricio for inviting me to be part of this such important joint session between Lars and Eira. Since the first subcutaneous ICD implantation in 2009 and the FDA approval in 2020, many improvements have been seen to reach the implant optimization as the evolution from the three incisions to two incisions surgery. Also, we expect the validation of the Pretorium trial, the Pretorium score, to reduce procedures timeout without DFT testing. Another sensitive improvement was the dual zone programming, as well as the third generation device, both reducing appropriated shocks to lower than transvenous ICD. So after understanding the difference between the surface seen by the subcutaneous ICD electrogram and its difference from surface ICD, and also the transvenous ICD that we usually see, the intracardiac signal, a screening tool has been validated, and a smart pass filter incorporated into the device. Next improvement came with better location of the components of a subcutaneous ICD. We do have the intermuscular position as the normally more used due to its unnatural position between the ceratus anterior and the latissimus dorsi. And in 2017, a large group did an evaluation of four different implantation techniques where four different implantation techniques were described. Then there was proposed to omit the superior parasternal incision. The lead insertion between the shift void and the pocket is identical. The difference in the parasternal tunnel, here the electrode insertion too, is covered by an 11-frame peel-away shift, and the electrode insertion is tunneled from the shift void incision in a cranial direction over the sternum. The electrode is inserted into the shift, and then the shift is peeled away, leaving the electrode in place. Finally, the lead is sutured with a sleeve to the fascia at the shift void muscle to ensure adequate fixation without the distal fixation, as we do not have the superior incision. The next step that we have the expectation for the next year regarding implantation procedures comes from the praetorian DFT results, despite we have 1% chance to fail defibrillator therapy when you have a praetorian score, full praetorian score, less than 90 results. This is not, despite of that, you should not use the praetorian score as an alternative for DFT in cases when DFT testing is possible or is desirable. Testing DFT in ICD implantations, in subcutaneous ICD implantations, cannot be a device until you have the full praetorian DFT results that will be available in October 2024. Regarding the efficacy and the safety of the subcutaneous ICD, the current approach at this moment, we have more than 100,000 ICDs, subcutaneous ICDs, implanted globally, as well as we have more than 12,000 patients enrolled in incomplete, sorry, enrolled in incomplete ongoing subcutaneous ICD clinical trials, completed and ongoing. Those are the reason that we have the device from guidelines, class 1 and class 2A recommendations in guidelines for subcutaneous ICD implantation. The first prospective and randomized clinical trials that we have had to have the subcutaneous ICD versus transvenous ICD was the praetorian trial. This was designed for non-inferiority. And on this hypothesis, with respect to major adverse events, like inappropriated shocks and ICD-related complications, that would require intervention. The trial enrolled 849 patients between March 2011 and January 2017 with Europe and the United States. So it determined non-inferiority in composite endpoints, four times more lead complications and two times more device extractions for infections on transvenous ICD. Also, there was no significant, there is no significant difference in inappropriated shocks rates at 48% for the subcutaneous ICD to 4.1% for transvenous ICD. And the study used a shock rate, and the study used mainly devices from the time before 2016, that it was not the enabled MRI subcutaneous ICD who has the smart pass filter. And then we're going to drop this inappropriated shocks to a rate at 2.4%. Actually, the most important data from untouched trial is, was the big data that we have here, the importance is, was the population that was a sicker population, a cohort with sicker patients that had lower, lower left ventricle ejection fraction, lower than 35%. And these were, those were compared to made it to IRT, transvenous ICD. The study that observed and dropped rated 2.5% with a shock, inappropriated shock, and a very high successful conversion at 98.4% for all patients that received subcutaneous ICD. And the last but not less important, the ATLAS trial, that was the first prospective and runs the mice clinical trials head to head, designed to determine the superiority conducted by Dr. Geoffrey Healy in Canada, to determine superiority with respect to seriously related complication. The ATLAS met its primary superiority endpoint, demonstrating a high significance, sorry, 92% fewer serious lead-related complications for EMBLD compared to any manufacturer's single-chamber transvenous ICD devices. Because of subcutaneous ICD has high conversion efficacy over 99%, low rates of inappropriated shocks at 2.7% on the atlas, and avoid many serious complications associated with transvenous ICD, those are supporting the idea that the majority of patients at risk of sudden cardiac death without an indication for pacing should receive a subcutaneous ICD. Then we have since from the guidelines, the American guidelines in 2017, the class one indication for patients who meet criteria for an ICD, transvenous ICD, an ICD implantation that had no adequate vascular access and a high risk of infection as well as patients on dialysis. They should be directed to a subcutaneous ICD implantation. And we keep the same class two way indication for an implantation of a subcutaneous ICD combined with a patient that has no indication for a therapy for bradycardia, no pacemaker, no resynchronization therapy needed, as well as no ATP. Then to take some home message, the subcutaneous ICD has been shown to have complete comparable efficacy, reliability, and safety outcomes compared to the transvenous ICD for the prevention of sudden cardiac death in patients who do not have a pace indication. When recording an ICD for the primary or second, recommending an ICD for the primary or secondary prevention of sudden cardiac death, patients should be given the option of a subcutaneous ICD with a high level of recommendation in the absence of pacing indications, as well as the subcutaneous ICD may be preferred over the transvenous ICD in patients at a high risk for cardiac implantable electronic devices, device infection, those with limited vascular access, and patients on dialysis in the absence of pacing indication. The subcutaneous ICD may be preferred in younger patients who may need multiple devices and leaders throughout their lifetime, and in women who are at higher risk for transvenous ICD complications in the absence of pacing indications. It's important to emphasize that the subcutaneous ICD should be included in the shared decision-making process in addition to discussion about the transvenous ICD when offering an ICD therapy for the primary or secondary prevention in sudden cardiac death in patients who meet implantation criteria without pacing indications. Thank you for your attention. Next speaker is Dr. Christophe Leclerc, cardiologist, electrophysiologist, and past president of the European Heart Reading Association, and actual president of the French Society of Cardiology. He works at Rennes University Hospital in France, and we are really, really glad to have Christophe with us today because he will be also with us in two weeks in Acapulco, so please enjoy this presentation. Go ahead. Thank you very much, Mario. Thank you, Maurizio. It's really a great pleasure to be with you. It's my first time in Mexico and the first time in Mexico City, but as Mario told you, I will come twice in two weeks, but unfortunately I have to go back to France. I will not spend some vacation in Mexico. So for me, it was very important to attend your meeting because, as you know, there is a long history of friendship between Iran and Laos, and with Jose Moreno, it was not possible not to be here with you tonight with this very important last 23 Congress. So my talk is about condition system pacing, current state, and future change, and because of time, I just want to focus my talk about the CRT indication. This is my disclosure. So why do we need an alternative to bi-VPC? Because now we started bi-VPC in 1994, and we have a long history of CRT using biventricular pacing, and you know that this technique is very efficient to reduce mortality, mobility, to improve quality of life, and to reverse cardiac dilatation. However, despite the improvement with different technology, we still have some failure of left ventricular lead implantation, around 5 to 10%, and also we know that when you use biventricular pacing with a lead inserted into the coronary sinus, you pace at the level of the epicardium, which is not optimally physiologic, and probably a more physiologic pacing mode should be more efficient. Also, we know that the efficacy of CRT is depending on the phenotype of the CRT candidates based on cure rate duration, condition disorders, LBBB or non-LBBB, and so on. And also, importantly, especially for patients implanted with a CRTP, if you use the condition system pacing, it's less expensive because you just need the DDD pacemaker, and one lead less. So, is CSP ready for CRT candidates? Of course, in case of left ventricular implantation failure, it could be a very good alternative. Upgrade to CRT, why not? Non-LBBB patient, because we know that CRT is less efficient in these patients. What about LBBB patients? Patients with lower ejection fraction and AV block? Also, patients with a strategy of ablative pace. Just want to show you this case from my institution. We tried to implant left ventricular lead into the coronary sinus, but we didn't find the coronary sinus because there was an atresia of the coronary sinus with a small persistent left superior vena cava. And for this patient, I don't know what will you do, but for us, it was obvious that we need to use the condition system pacing because it was not possible to cannulate or to go into the coronary sinus. So, what is condition system pacing? We started condition system pacing many years ago in the early 2000s with Dr. Desmuk, with his pacing. But condition system pacing today is not only his pacing. It could be also LBBB pacing, which is not very used, but also left bundle bronchial area pacing, including LBBB pacing, left ventricular septal pacing, and left fascicular pacing. So, when we discuss about condition system pacing, today we discuss more about LBBA pacing, that is pacing, because his pacing is a little bit, I will not say out of the game, but less used than before. So, what did we wrote in our guidelines at the ESC with ERA in 2021? We have very few indication for a CSP pacing because at this time, we didn't have a lot of data. We just considered that his bundle pacing could be an alternative if we were in the case of we have a non-successful implantation of the left ventricular bit. But at this time in 2021, we didn't mention any indication for LBBA pacing because we didn't have enough data at this time. We will see that our colleagues from Latin America, HRS, have new guidelines for that. But by the way, when you look at this survey performed in Europe, you can see that LBBB pacing is already very adopted by a pacemaker or physician in patient with AV block and ROQRS. It's about 50-50 between his pacing and LBBB pacing. But if you move to a failed biventricular CRT, you may appreciate that most of the physicians, about 60% of them prefer to implant LBBA pacing. And it's the same with slowly conducted AF, AV block with YQRS, sinus node disease, it's mixed 50-50. But when you have a bundle branch block and low AF, once again, LBBB pacing is the most adoptive technique for conduction system pacing. So, what do we have like evidence? In fact, we have very, very, I would say, no very strong evidence about conduction system pacing in patient with CRT indication. I will show you some example and you will see that all it's observational data or it's randomized trial, but very, very limited number of patients. And this is one of the first trials, the IS-SYNC, and you may appreciate that only 40 patients were included in this trial, 21 in IS bundle pacing group, 20 in BIV pacing. And you may appreciate also that there was a huge crossover between IS bundle pacing to CRT, but also between BIV pacing to IS bundle pacing. By the way, when you look at intention to treat, you can see that you have a significant reduction in both group and the magnitude of reduction was much better with IS pacing as compared to BIV pacing. And you have also a larger increase in left ventricular ejection fraction with IS pacing as compared to BIV pacing. And if you look at IS treated, you may appreciate that you have a significant reduction in QRS duration and are more patient with an increase of at least 5% in left ventricular ejection fraction. So, small study, lot of crossovers, but interesting data. Now, this is another survey conducted in about 100 patients. The patient had a left ventricular lead implant failure. There were non-responders to CRT of their primary CRT indication, so it was a mixed population. You may appreciate that with IS pacing in this study, we have an increase in pacing threshold in about 7.5% over six months follow-up. And you may appreciate that in every type of patient, we have a significant reduction of the QRS duration, patient with bundle branch block or patient with a pace in the ventricle. For patient with narrow QRS, there was no significant difference between before pacing and after pacing. Once again, an improvement, a significant improvement in left ventricular ejection fraction with IS pacing and also a significant decrease in the NeuroCard association class. So, also encouraging data for IS pacing. And the last one was published two years ago. It was also a small study, 50 patients randomized in two groups, 25, 25 in each group. And you may appreciate that between by the pacing and the IS pacing, there was no significant difference in terms of change in the QRS duration, NeuroCard association class, left ventricular ejection fraction, or left ventricular anesthetic value. But now, as I told you, we use more and more left bundle branch area pacing. And this is a very interesting survey from Europe published last year, including more than 2,500 patients from 14 European centers, very trained centers for LBBA pacing. And so, you can see that in the majority of the case, the pacing was at the left branch fascicular posterior area. There was some failure, of course. And interestingly, when you have an indication for bradycardia, the success rate in these very experienced centers is 92%. But if you move to the CRT population, so a patient with heart failure, you may appreciate that you have a decrease in the success rate to 82%. Of course, we have a complication as a very invasive technology. But you may appreciate that we have new complication we didn't have before with the other technique, because it's acute perforation to the left ventricle. However, heart failure indication was a risk factor of failure of implantation of LBB area pacing. Interestingly, also, if you start your experience with LBB pacing, you should understand that there is a learning curve, and the learning curve is about 20 implantation. After only 20 implantation, you become comfortable with LBBA pacing. So, what do we have like data? We have this survey from Dr. Vizhar Piaget-Aliaraman, 325 patients with low ejection fraction below 50%, an indication for CRT or pacing. The success rate of LBBA pacing in this very experienced center was 85%. And you may appreciate that in terms of cure duration, New York Heart Association class, there was absolutely no difference between LBB and non-LBBB patients. Also, for left ventricular ejection fraction and left ventricular and diastolic diameter reduction. So, very interesting technique improving cure duration, left ventricular ejection fraction, and reverse remodeling, as well as functional status. We have this trial published last year by Dr. Wong, who is, I would say, the father of LBB pacing. Once again, it's a very small study, 40 patients with non-encechemic cardiomyopathies that are randomized in two groups. There was some crossover, 20% crossover from BIV to LBB pacing, which is a little bit surprising for me. And LBB pacing, it was a 10% crossover to BIV pacing. By the way, there was an advantage in favor of LBB pacing as compared to BIV pacing. In the main outcome, which was left ventricular ejection fraction, we have higher increase in left ventricular ejection fraction. You have also a more pronounced cure duration reduction. There was also same result for left ventricular reverse modeling, and also anti-proBNP. This is a study comparing matched control group with a patient with CSP. It's not a randomized trial, so they included 500 patients. And you can see that if you look at the outcome, strong outcome, death of outflow hospitalization, you have a significant reduction by 40% for CSP as compared to BIV pacing. And if you focus on the right part of the slide for LBB patients, you have also a significant benefit for CSP pacing as compared to BIV pacing. But it was not a randomized trial. So, okay, it could be done for every indication, but we have to be very cautious because it's based on no strong data for me. If you want to read more about that, you have this paper published in conjunction with APHRS, Canadian Autism Society, and LARS about a very practical guide how to do LBB pacing. If you want to implant or to be sure you're in the LBB area. I just want to remind you that now the EP European Journal is an open access journal, so everybody may have access to that. So, our colleagues from HRS, APHRS, and LARS published this year during the meeting in New Orleans guidelines on cardiac physiologic pacing based on the new data we have now since the publication of the ASC guidelines. And I just want to show some slides for patients with LBB, YQRS, and a patient in Neuropathic Association class 2 to 4. CRT is still in green with a class 1 indication, but you can see that CSP with ease or with LBB correction or LBB pacing is reasonable if CRT cannot be achieved. So, two indications. And also, it become for the other patient, it's the door is open with a 2B indication. If you look at patient with non-LBBB and courage duration over 150 millisecond, it's a 2A indication for CRT for Neuropathic Association class 3 to 4. But for patient with class 2, it's a 2B and you may implant CRT or conduction system pacing devices. And finally, for non-LBBB and QRS below 150%, it's a 2B indication for CRT or conduction system pacing. And in fact, there is no benefits proven today in patient with narrow QRS, less than 120 milliseconds, whereby the pacing is not recommended and there is no data for CSP pacing as well. So, to conclude, I would say that conduction system pacing and especially LBB area pacing is very promising for every CRT candidate. But I think that we do need to have a proof of at least non-inferiority and if possible superiority with strong evidence-based medicine. And I put in this table all the trials we were performing with BIV pacing. And if you make a calculation, 25,000 patients were included. So, we have very strong evidence for BIV pacing and for CSP today, it's a little bit weak, I would say. This is just a global picture of the clinical trials which are ongoing in different typology of patient. Patient with wide QRS and low ejection fraction. Patient with intermediate ejection fraction, wide QRS. Or patient with normal ejection fraction with heavy block. And you can see there is a lot of trials. And the results should be expected in two or three years. Perhaps we don't have to oppose BIVI pacing and CSP. Perhaps we can combine left ventricular pacing and CSP. And this was the purpose of the low CRT trial. We did show that when you combine CSP and BIVI pacing, you significantly further decrease the QRS duration as compared to LBBA or BIVI pacing. And probably this is a very interesting technique, a little bit more complex, but interesting, which we'll be assessing as a follow-up. So I would like to conclude. I hope that we will see most of you in Berlin in April. I don't know if you know Berlin, but it's a very attractive city. And I hope that you will attend the Iraq 2024 Congress between 7 to 9 April. Thank you very much for your attention. And now we'll move on to the last presentation. We invite Dr. Jose Carlos Pachon, a cardiologist, electrophysiologist, and arrhythmia director of the Hospital of the Heart of Sao Paulo in Brazil. He is the ideologist and the father of the cardinal ablation. And that's one of the new jewels in electrophysiology. And he will talk about the state of the art of the cardinal ablation. Thank you. Good morning, ladies and gentlemen. It's an honor for me to be here, participating in this event. Thank you very much, Dr. Mauricio, Dr. Maglio. I would like to congratulate Dr. Ulisses for creating, for organizing this meeting, this outstanding meeting. I would like to do my greetings to Dr. Marino, Dr. Leclerc, representing one of our modern organizations, ERA. It's an honor for all of you to have them here. I would like to talk about cardinal ablation, the state of the art. I have to show some basic concept, because obviously there are several people that probably didn't see this subject. So it's necessary to show something basic. And I would like to ask for our presenters to subscribe to the Second World Congress of Cardinal Ablation. We are organizing it next Saturday in the United States. And this is a free meeting. And obviously, it will be very interesting for all of you that like this new field in electrophysiology. We have nothing to be disclosed. And the origin of the cardinal ablation was it was created during our studies about the substratum of atrial fibrillation in the 90s. We were studying the origin of the cardinal ablation in normal people. So we used it to study the atrial potentials with spectral analysis. And we can see here the spectrum. And we found that there are two kinds of spectrum in the atrial myocardium, the compact myocardium that is composed with cells very well connected, and the fibrillar myocardium that is composed with loose cells, with disconnected cells without fibrosis. There is no necessary fibrosis to explain the origin of atrial fibrillation in normal heart. So in that time, we found that the fibrillar myocardium were caused by intrinsic of the pulmonary veins and of the innervation of the heart. We gave the name of atrial fibrillation nest to the clusters of fibrillar myocardium that is easy to get mapping on the recordings, conventional records, or obviously by the spectral analysis. We found that the ablation of the AF nest caused two consequences. The first one is that the atrial became completely resistant to reinduced atrial fibrillation. The atrial became resistant to instability, to electrical instability. And the other consequence is that the atrial became denervated. So in that time, we observed that AF nest ablation caused the denervation. So based on this finding, it was possible to create the cardioneuroablation procedure to eliminate the innervation of the heart. We have here an interesting trial that was published by Dr. Enrique Pachon, showing that the ablating atrial outside of AF nest caused no denervation, while ablating atrial in atrial fibrillation nest caused complete denervation. It is very clear, and it was published in circulation. In that time, in the 90s, we decided to create this procedure, aiming to denervate the heart in order to treat several conditions that are originated by increasing of the vagal tone. About the technique of the cardioneuroablation, here we can see an ischemia of the autonomic nervous system of the heart. We can see in yellow the parasympathetic system and in white the sympathetic one. We can see that only the parasympathetic motor system presents the postganglionic neuron in the atrial wall. It is extremely important. It is extremely important, because if the neuron is located in the atrial wall, it may be eliminated by the RF energy. It is easy to eliminate it, and cause, obviously, denervation. Otherwise, the ablation of the sympathetic neurons is not possible, because the neural body are located far from the atrial wall, far from the heart. So there is a selective parasympathetic denervation. In that time, we observed that most of the denervations are related to the locations of the ganglionate duplex sites in the heart. The first one located between the insertion of the, between the aorta and superior vena cava. The second one located in the insertion of the right pulmonary veins. The third one in the insertion of the coronary sinus. And the fourth one in the insertion of the left pulmonary veins. In that time, in 2005, we developed the fractionation mapping. In order to map the innervation, you know that it is not possible to map the action potentials of the neural system of the heart. So in that time, we developed the fractionation mapping in order to get an approximation of the spectral analysis of the atrial wall. And the fractionation mapping nowadays is used by Abbott in their electroanatomic system. Here, we can see that the green areas are areas with high probability of innervation, and the purple areas are areas with low probability of innervation. And here, we have an example. We have no time to explain, but there is an example of one case that were completely denervated from the sinus node and the AV node. We have also denervating even the atrial wall in order to treat atrial fibrillation. So obviously, the denervation may be very short and may be very extended, depending of the aim of the procedure. In order to study the denervation during the procedure, we develop the extracardiac vagal stimulation. And this procedure is based on the placing of catheter inside of the internal jugular vein near to the jugular foramen. In this point, it's possible, with the specific adjustments of the stimulator, it's possible to get the vagal stimulation without contact by field effect. And here, we can see the asystole induced by the vagal stimulation. And after this, after the cardioregulation, there is no more asystole, showing that the procedure was well-succeeded. Here, we can see an example showing a patient presenting vasovagal syncope, showing the long asystole caused by the vagal stimulation. And after the cardioregulation, by stimulating the vagus in the same place, it is clear that there is no more vagal effect. We can see that the vagal stimulation causing no more bradycarria, no more heavy blocks, no more asystole. It makes possible to get a good endpoint to the procedure, a rational endpoint to the procedure. Based on this procedure, nowadays, we have the rational cardioregulation. And obviously, if the procedure is not performed, we have the empirical cardioregulation. Here, we compared the results of a group of patients submitted to cardioregulation with vagal control and in red, cardioregulation without vagal control. It's clear that the results, the recurrence of syncope is higher in the group without vagal control. It is extremely clear, because the difference is in order of five times. About the results, in the first publication in the 90s, in patients with neurocardiogenic syncope, functional high-degree AV block, sinus node dysfunction, and atrial fibrillation, all of these conditions were related to vagal hyperactivity. And obviously, it's very important the patient has no cardiopathy. The cardioregulation was developed to treat the functional conditions. And here, the first trial that was performed by Dr. Piotrowski in Poland, showing that the cardioregulation shows a very better result than clinical treatment in neurocardiogenic syncope. They showed very, very good results. And here, our results. Here, we can see the cardioregulation, the empirical cardioregulation in red. And in blue, there is the cardioregulation controlled by vagal stimulation. Here, the clinical treatment that was published by Dr. Roman. Here, the cardioregulation in the group of Professor Roman with very good results, obviously with a short follow-up. And here, the best study we use in pacing, the Spain study, showing that the pacemaker is a good option for treating neurocardiogenic syncope. However, they presented a short follow-up. We have a very long follow-up. And here, some examples. An example of functional AV block with syncopal functional AV block, completely treated with cardioregulation without pacemaker implanting. Here, a study showing that the cardioregulation is showing even better results than pacemaker. It was published by Dr. Rakesh. But I think it's necessary to have a longer follow-up. There are a lot of trials that have been showing short follow-up. I think it's not right for the procedure. Here in our service, Dr. Hortensio showed that the pacemaker implantation in functional bradyarthritis was necessary only in 18% of patients. So near 82% of patients were treated without pacemaker implantation. And here, a study in our service that is ongoing with Dr. Zerpa showing that the cardioregulation presents a very good result in patients with carotid syndrome in very well-selected patients. Here, the indications of the cardioregulation. We can see that all the reflex bradyarrhythmias and even functional non-reflex bradyarrhythmias are very well indicated for cardioregulation. And one of the most important is atrial fibrillation. We have been observing very, very good results with cardioregulation in atrial fibrillation ablation. We have only 8% of complications, but you can see that all of these complications are for very easy treatment without surgery. And obviously, the last question, is there any risk resulting from the cardioregulation vagal tonic reduction? It is a very important question. We know that the very critical cardiopathy evolves with low vagal activity. However, it is an association. It is not causing effect. It is very important to have in mind. So in our study, we observed that after cardioregulation, two years after cardioregulation, there is a very important reduction of the parasympathetic tone and also reduction of sympathetic tone. In cardiopathy, there is increasing of sympathetic tone and the reduction of the parasympathetic tone. Here we can see that in atrial fibrillation, all well-succeeding atrial fibrillation ablation is followed by atrial denervation. We have a lot of trials showing this. And we have now a lot of trials showing that atrial fibrillation causes reduction of the mortality. So the vagal denervation is not cause, is not reason to increase mortality. The studies are showing reduction of mortality. And at the end, it's very important to see here in red, the sympathetic tone, and in blue, the parasympathetic tone. The relationship between two tones, we can see that the normal patient presents sympathetic tone and parasympathetic tone. We can see in the right superior quadrant. And during the sleep, during the rest, we go down to the right inferior quadrant with high parasympathetic tone and low sympathetic tone. In cardiopathy, we are in the high left superior quadrant. Post-MI, for example, and cardiomyopathy with low ejection flashing. In this case, there is high risk because there is low parasympathetic tone with high sympathetic tone. And during atrial, after cardioregulation, we are in the inferior left quadrant, presenting low parasympathetic tone and low sympathetic tone. So in our studies, we are studying these more than 25 years. We have been observing no reduction, no increase of arrhythmias, and obviously, no increase of mortality. Here, we can see a study of 83 patients followed by two years. In this group, it was very clear and very significant reduction of supraventricular arrhythmias, reduction of ventricular arrhythmias, and reduction of albrady arrhythmias. So in our studies, the cardioneuroblastion is not arrhythmogenic. It is a safe procedure. Thank you very much. Thank you very much, Dr. Pachon, for this excellent talk. We are on time, so we will have questions this time. But you can approach the speakers, please. They are welcome to receive your observations or comments. I would like Mauricio to close the session, please. Thank you. Thank you so much for the wonderful presentations. Now, we'll move to the next session that I think it's starting now. We're a little late. Thank you. Thank you for the presence. Thank you.

electrophysiology

radiofrequency ablation

needle ablation

cryo ablation

subcutaneous ICD implantation

cardiac arrhythmias

atrial fibrillation

neurocardiogenic syncope

ventricular arrhythmias