I'm Kumar Narayanan from India, I'll be, it's my pleasure and honor to chair this session on advances in ICD technology. So we have five oral abstracts and each presentation is for ten minutes, I request the speakers to stick to time and then we have two minutes for questions and answers after that and you can ask your questions to the speaker after they present and I would request the speakers to please repeat the question once into the mic so that all the people wearing headsets can hear them and then to give the answer after that. So with this I would like to call upon the first speaker Dr. Karim Saleh to talk about the EVICD. So good morning ladies and gentlemen, dear colleagues, dear chairman, thank you very much for the kind invitation and giving me the opportunity to share my experience in EVICD implantations in pediatric patients. These are my disclosures, since decades transveners ICDs are the gold standard of the therapy of device-based therapy for preventing patients from sudden cardiac death. Anti-tachycardia pacing is an important advancement which can reduce shocks which are sometimes appropriate but sometimes unnecessary and painful. The transvenous ICDs also have complication rates, high complication rates like venous occlusions, lead fractures, infections especially in younger patients. The subcutaneous ICD was designed and developed to minimize these complications by sparing the vasculature system and limit these complication rates. But the subcutaneous ICDs also have limitations like higher shock energy required and resulting in a bigger can and a shorter battery life and ATP cannot be delivered. So what are our approaches and possibilities to implant EVICDs in pediatric patients? We have invasive approaches which requires anatomy which can be done by patches or like here with dual coil ICD electrodes slinging around the heart. This is very invasive. We can do transvenous ICDs but they have a high complication rate in our pediatric patients and we can do subcutaneous ICDs. And here the limiting factor is the size of the can. So all of these possibilities are not evaluated especially for pediatric use and so there is no optimal alternative on label. All of our options are off label. So the extravascular ICD, EVICD Aurora from Medtronic is commercially available since September 23. The electrode is positioned substernally and so there is a close relationship between the electrode and the heart and so the device can provide defibrillation with low shock energy, can provide anti-tachycardia pacing, post-shock pacing and post-prevention pacing. This with a can size that corresponds to our normal transvenous ICDs with a longevity of approximately 12 years. So pediatric patients have high device related complication rates with transvenous ICDs and they could and may therefore particular benefit from an EVICD. However, it's used in children and adolescents has not yet been tested in a structured manner and is therefore off label and not approved. So in our single center case series we implanted five children or pediatric patients with an EVICD between December 23 and August 24. The median age was 15 years, a range from 7 to 17 years with a median weight of 60 kilogram, 23 to 60 kilogram and a median height of 162 centimeter, a range of 136 to 170 centimeters. The underlying cardiac conditions were hypertrophic cardiomyopathy in two patients, long QT syndrome in one patient, arrhythmogenic right ventricular cardiomyopathy in one patient and idiopathic ventricular fibrillation in one patient. The median procedure duration was 83 minutes with a median fluoroscopy time of five minutes, R wave amplitudes, stimulation impedance, shock impedance and threshold values were within expected ranges for adults. So in our implantations we had no intra and no peri procedural complication so far. Now there's a short case report about our youngest patient. He was a seven year old boy with a height of 136 centimeter. He weighed 22.5 kilogram and he lost consciousness in July 24 when he was swimming. They resuscitated him and it required three shocks to terminate the tachyarrhythmia with a 95 joule shock. ECG, echo, CT scan and MRI were quite normal. The EP was, there was no tachycardia inducible. The femoral history was negative so we saw a class one indication for secondary prevention. We made a CT scan, I had a look at a CT scan and we could see that the right pleura shifted to the left. That's not quite normal in pediatric patients and I measured the distance from the carina to the siphisternal junction and it was about 8.5 centimeters so I thought maybe it's feasible to do an implantation with an EVICD. I do all my EVICD implantations in general anesthesia in the hybrid OR. First when I begin I do draw my landmarks as you can see here. Then I do washing and draping and then I do the first incision, a small incision left to the siphoid process and then I do the blunt finger dissection. In younger patients, especially in pediatric patients, it's very hard to do the blunt finger dissection because they have a very tight and strong tissue. In the beginning I tried to use my digital finger then I had to switch to my smallest finger. In the end I ended up with this dissecting swab fixed to the sponge forceps so I could get access to the anterior medial stynum. The tunneling, substantial tunneling was quite easy, it's straightforward. I did it in two steps. As you can see in the middle the tunneling was quite fast and I went high up. I wanted to reach the carina level as upper level and a little bit more just to be safe. And you can see the final position, I withdrew the tunneling rod, the safe sheath stays inside. I used the defibrillator lead and pulled back the safe sheath so the lead could develop his typical epsilon shape as you can see here. Then I sutured the lead to the erectors fascia, I created my pocket in the lateral wall and then I tunneled to the left and connected the device with the electrode. Our measurements, we had a duration of 83 minutes, the fluoroscopy time was 3.2 minutes, R-Wave 2.4. The impedances were great, the threshold 3 volts at 4 milliseconds and we did DFT testing. In this DFT testing we had three inductions but in all our VF episodes we had a spontaneous termination. After six weeks we had a follow-up and as you can see the cosmetic result I think is quite fine. The patient was fine and X-ray as well. Four months later there was an episode, again loss of consciousness at the playground. As we did the follow-up we could see that the device detected the VT, the fast VT correctly. There was a shock with a 41.8 joule, successful and it terminated the arrhythmia. So in conclusion, the Aurora EV ICD system is approved for the treatment of malignant cardiac arrhythmia in adults. It prevents vascular complications and enables ATP with a comparatively small can and a long bodily life. Young patients with transvenous ICDs are at considerable risk of complications and could particularly benefit from this new technology. Implantation in our five pediatric patients was performed without acute complications and it is currently not clear whether positioning the electrode in the mediastinum could have adverse consequences on local infections or necessary future extraction. To date there is no case of mediastinitis described, neither in our series nor in the entire pivotal study cohort. Thank you very much and I'm happy to take questions. Thank you. Are there any questions from the audience? Dr. Salih, maybe I can ask you one question. I hope you are able to hear me. So you told me the target as well as the threshold, so they seem to be quite different from what you encountered with transvenous ICD. Have you experienced extra-masculine ICD or is that different in children? The question was about the R-wave and the measurements in EVICDs. Generally in EVICDs we expect R-waves above 1 millivolt. So we are satisfied with 1.5 and we do not accept P-waves. The correlation should be not much more than 10% between R-wave and P-wave. But it's different to our transvenous systems. In transvenous systems we expect 10 or more millivolts. In our EVICD we are satisfied with 2 or at least 1 and 2.4 is great. Generally in pediatric patients I could see that they have a little bit higher R-wave than adults. And in terms of the threshold, in terms of the basic threshold, who was the most likely to get 3 volts? The question was about the thresholds. The thresholds are sometimes high. We don't know in which patient we could expect higher thresholds, but it's not an issue in the implantation. We always have captured sometimes very high thresholds, but we do not focus on that. We always focus during the implant on sensing, that's the main point. And pacing, it's not a pacing indication, it's only for ATP, a rescue ATP to save the patient from a shock. And sometimes they have sensations about the ATP. So it's not comfortable for them, but I think it's necessary to use it because it avoids them from shocks. Yeah, another question? The question was about the positioning of the lead. It looks shifted to the left. That's normal, we always want to be to the left, because we do not want to go midline. There's a lot more risk of complications when we use midline. We have the syphoid process, which is sometimes very variable and long, and so we are not getting access to the mediastinum if there is a long syphoid process. And you can get into the right pleura, but you have more complications and risks of perforating into the pericardium. So the best position and tunneling is a little bit switched and shifted to the left of the syphoid process. There's a margin between the costal margin and the syphoid process, and in this angle you should start tunneling. Thank you. Yeah? The question was about dislodgement during exercise, and that's a main point. You should focus on fixed suturing during the implant, that you have no dislodgements, because they are exercising, they are young, and if you do your sutures exactly and precisely, they can do whatever they want, it won't dislodge. Thank you. Thank you very much. Thank you, Dr. Saleh, for that excellent presentation. We'll move on to the next case, the next substrate by Dr. Claudio Suja, who's going to talk on the MADIT-ICD benefit score. Thank you, Mr. Chairman, ladies and gentlemen. My disclosures here. It's taking a while to load. Okay. On behalf of the steering committee of the APPRAISE-ATP trial, it's my pleasure to present to you the MADIT-ICD benefit score in the modern era in sites from APPRAISE-ATP. The benefit of ICD primary prevention patients have been established by landmark randomized clinical trials performed two decades ago, as shown in the graph. However, the use of current guideline medical therapies have called into question the utility of prophylactic device implantation, and it's not surprising that more refined re-stratification has been proposed to identify primary prevention patients more likely to benefit from ICD implantation. The MADIT-ICD benefit score, published in 2021, has been proposed to elucidate the competing risk of arrhythmic and non-arrhythmic mortality to determine the utility of primary prevention ICD implantation. Utilizing the MADIT family of ICD trials, 4,500 patients were retrospectively evaluated to identify risk factors associated with ICD treatment for VTVF above 200 beats per minute and its counterpart, non-arrhythmic death, as shown in the table to the right. A weighted score was adjudicated to those individual risk factors identified as predictive of treated VTVF events and or predictive of non-arrhythmic mortality. CRTD patients received a negative score of minus one given the reduced overall mortality in eligible patients. A matrix then constructed, shown to the left of the slide, based on patients' VTVF and non-arrhythmic mortality total scores to assess the probability of ICD benefit. The lowest MADIT ICD benefit group in red have a low score for VTVF and high score for non-arrhythmic death, which translated in a low ICD benefit score of zero to 25. On the other extreme, the highest MADIT ICD benefit group, depicted in green, included patients with high VTVF scores and low non-arrhythmic mortality scores, which translated in the highest ICD benefit score between 76 and 100, with an intermediate benefit group scoring from 26 to 75. This slide shows the performance of the MADIT ICD benefit score in the MADIT trials. The highest benefit group to the left, which scored between 76 to 100, had a high incidence of treated VTVFs and a lower chance for the competing risk of non-arrhythmic mortality. The lowest benefit group in the graph to the right, which scores between zero and 25, derived no benefit due to a higher incidence of non-arrhythmic mortality and a low incidence of VTVF during follow-up. We need to emphasize that in the MADIT family of trials that included CRTD patients, there were different programming in each of the individual trials going from physician discretion programming in MADIT II to only one second delay prior to therapy in the MADIT CRT and from one second up to 12 seconds delay prior to therapy in the MADIT RIT trials. As a result, treated VTVF events above 200 beats per minute definitely included self-terminating episodes, so its utilization as a surrogate for potential arrhythmic death and hence ICD benefit may have been overestimated. Based on the prior considerations, we decided to test how the MADIT ICD benefit score will perform in a large, uniformly programmed group of primary prevention ICD patients. The APPRAISE ATP trial was a very large randomized trial evaluating the value of ATP in primary prevention patients. Above 200 beats per minute, all patients have uniform programming with long therapy delays of 12 seconds prior to the randomized arm of first therapy delivery, either ITP or shock. And above 250 beats per minute, all patients, irrespective of the randomized arm, receive a shock after a five-second delay. In summary, therapies were uniformly delivered after a very significant delay, representing a better proxy for a putative, sustained, and potentially lethal ventricular arrhythmia. The objective of the analysis was to assess the utility of the MADIT ICD benefit score in stratifying the risk of VTVF versus non-arrhythmic death in a large, contemporary patient cohort with modern programming parameters and current guideline-directed medical therapy. A total of 2,475 appraised ATP patients were successfully assigned an individual Mated ICD Benefit Score. The number of patients in each Mated ICD Benefit Score category is shown in the graph, with most patients scoring in the Intermediate Risk category. Now to the results. To the left is the rate of treated VTBF above 200 beats per minute, and to the right the rate of nonarrhythmic death in the appraised ATP cohort. Patients are grouped according to their assigned Mated ICD Benefit Score in color-coded fashion. In the graph to the left, the percentage of patients treated for VTBF in each Mated ICD Benefit Score is shown. The percent of patients with treated VTBF was highest in those with the lowest benefit score, shown in red, while the Intermediate in black and the highest benefit group in blue were bunched together with a lower percentage of treated VTBF events in total discrepancy with their assigned Mated ICD Benefit Score. However, for the rate of nonarrhythmic mortality, the Mated ICD Benefit Score performed well, maintaining its assigned priority with the lowest ICD Benefit Score in red, having the highest incident of nonarrhythmic death and the highest ICD score in blue, the least. The bar graph indicates the lack of correlation in the incidence of treated events between the Mated ICD Benefit Score in Mated cohort in green and in the appraised ATP patients in blue. The overall rate of delivered therapy was markedly lower in appraised ATP than those reported in the original Mated ICD score, analysis at three years of follow-up. Programming differences, namely therapy delays and progress in medical therapy between the legacy Mated trials and the appraised ATP trial, reduced unnecessary therapies in general and specifically for non-sustained events affecting the predicting value of the score. As opposed to the poor predicted value of the Mated score in predicting treated VTBF, the score performed well in the prediction of nonarrhythmic death in the appraised ATP trial shown in blue. As can be seen in the bar graph, nonarrhythmic mortality rates maintain the priority order according to their assigned scores in correlation to the Mated ICD Benefit Score. The cumulative incidence of nonarrhythmic death at three years of follow-up was significantly higher in appraised ATP, most likely because appraised ATP did not include CRTD patients shown to reduce overall mortality in eligible patients. This graph aims to show the overall benefit of ICD implantation in the appraised ATP trial. In the first row, we show patients that received appropriate therapy and survived to the end of the follow-up. A total of 7.6% of patients received therapy in the appraised ATP trial and survived to the end of the trial with a calculated 23 mean months of life gained. The second row shows patients that received therapy but did not survive to the end of the trial and have a calculated mean life benefit of 10 months. The third and fourth rows show patients that never received therapy and survived, 78%, or died a nonarrhythmic death, 12.4%, and hence derived no benefit from device implantation. For the full patient cohort, the mean life months gained was only two months. In conclusion, although ICD benefit was established for a limited group of primary prevention patients required device intervention, the mated ICD benefit VTVS score lacked the ability to identify these patients in the appraised ATP cohort. Modern programming techniques with extended therapy delays contributed to a decrease in premature and unnecessary therapies, resulting in a significantly lower number of therapies delivered in the appraised ATP trial compared to those observed in the mated ICD trials. These variants influenced the performance of the calculated mated VTVS score that interpreted therapies delivered as a proxy for potential ICD benefit. The identified risk factors in the mated ICD benefit score for nonarrhythmic mortality appear validated in the appraised ATP trial. The use of the mated ICD benefit score required re-evaluation in the context of modern programming recommendations and guideline-directed pharmaceutical, and the identification of novel risk factors is needed to predict arrhythmic mortality and ICD benefit. Thank you very much. Excellent presentation and I think the issue of competing risk I think is very important. So, also the overall net months gained was quite low, so what's your overall feeling now about the primary prevention of ICD in general and what is the current level of 3DMT benefit? The question specifically is that overall for the population, the benefit in mean life gain is pretty modest. And this is a fact. It's a fact that it's known to us and has become known to us in the recent future even more with current guideline medical therapies. 90% of patients, 90% of implantees do not derive benefit of their ICD. That is the starting point in which we all have to operate. Now surprisingly in the trial, 7.6% of patients derived quite a benefit from the ICD. However, those are the patients that interestingly have a high competing score for nonarrhythmic mortality as well. So, the issue that becomes a quandary is how to peel those patients from those in that category of score that will not benefit from the ICD and we are not there yet. We are working to try to identify risk factors, but we are not there yet. The important thing is that the paradigm shift of implantation of ICD has to change in terms of what is the most important part of an ICD implantation and in my opinion, the most important part is the safety of the platform you are using more than the benefit because you are implanting 93 patients that are never going to use their device for 7 or 8 that were actually going to use it. You are talking the arrhythmic mortality risk of the mated ICD benefit score? The nonarrhythmic of the mated ICD benefit score? No, I do not know the answer to that question, however, you know, the paper was published In your data, you had 13 to 14.5% nonarrhythmic mortality, that's not probably very statistically significant. That is correct. It was not very statistically. You are talking about appraised ATP now, okay. Yes, it was not very statistically significant, that is correct. Thank you. We will move on to the next talk by Dr. Michael Kletcher on the Improved ICD Shock Efficacy. Good morning, I would like to thank the Heart Rhythm Society, the chairman and the audience here for inviting me to present our study, Improved ICD Shock Efficacy Using Programmable Pulse Width. These are my disclosures. For decades, implantable defibrillators have used biphasic waveform to defibrillate. This is a two-phase approach in which the first phase delivers optimal shock energy to capture critical mass of the ventricular tissue to terminate ventricular fibrillation. The second phase, reversing the polarity, will remove excess charge from the tissue to prevent reinitiation of arrhythmia, commonly referred to as the burp effect. There are two key components to a biphasic shock. First is the pulse width of each phase measured as duration of each phase in milliseconds and the tilt. Tilt is defined as the percent drop in voltage across each phase. Here is an example of a 65% tilt. Conventionally, devices are programmed with fixed tilt. Abbott devices allow reprogramming of devices either in fixed tilt or in fixed pulse width. When fixed tilt is chosen, a specific energy is delivered. Duration of that shock will vary depending on the impedance. In contrast, fixed pulse width assigns a voltage and, as such, current delivery in each phase for a specific pre-programmed duration. Devices cannot be programmed fixed tilt and fixed pulse width at the same time, obviously. There are advantages of a tuned fixed pulse width. The goal of the first phase of the biphasic shock is to maximize cardiac cell membrane voltage changes to terminate ventricular fibrillation. By tuning the waveform and specifically truncating the first phase, this maximum energy can be delivered without delivering excess energy, as excess energy can be potentially arrhythmogenic and deleterious. The second phase is also timed in the reverse polarity to remove excess charge without delivering excess energy in the reverse polarity, applying more energy, which, again, can be proarrhythmic and damaging. This can be programmed easily with the Abbott devices using the fixed pulse width programmability feature known as the precision shock technology. The device is programmed either fixed pulse width or fixed tilt, and when fixed pulse width is chosen, the duration of each phase is chosen based on an algorithm. There's been prior clinical evidence showing the efficacy of fixed pulse width at DFT testing at implant. Denman et al. showed in a series of 54 patients a drop in defibrillation threshold of 20% when using fixed pulse width. Mujawar et al. in a slightly larger series showed similar defibrillation thresholds when patients were tested in both modes, however, in the group with high defibrillation thresholds defined as greater than 400 volts, there was significant reduction in defibrillation threshold. As such, fixed pulse width may provide lower DFTs, especially in outliers with high defibrillation threshold. However, until now, we haven't had real-world intrapatient comparison of fixed pulse width versus fixed tilt in the same patients who have had clinical episodes treated with both episodes rather than at implant DFT testing. To do that, we went to Merlin.net and reviewed the database. Our objective was to compare shock success rates and energies for ICD devices programmed with both, identifying patients who, during their clinical experience, had both fixed pulse width for a time and fixed tilt for a time and who received shocks for clinical episodes with both modalities. Our methods were to review the database, the Merlin.net database, in patients with single or dual-coil ICDs listed here, and identify patients who, throughout their clinical experience, were programmed for some time with fixed tilt and for some time with fixed pulse width. And these same patients were identified who had at least one shock-treated episode for fixed pulse width and at least one shock-treated episode for fixed tilt. Paired intrapatient differences in shock success rate and delivered energies were evaluated across all shock-delivered episodes for each patient. So let's look at our patient characteristics. We identified a total of 295 patients who, during their clinical experience, had a time in fixed pulse width mode and a time in fixed tilt mode and who received at least one shock episode with programming each of these features. The demographics included an average age of 70, 87% of our patients were male, 44% of our patients had CRT. The important question is, how were these patients programmed? 77% of them initially were programmed fixed tilt, which is the typical convention, and they were subsequently programmed to fixed pulse width. 22% of our patients were initially programmed fixed pulse width and were subsequently programmed fixed tilt in their clinical experience. The mean number of shock episodes delivered for patient was two shock episodes per patient while they were programmed fixed pulse width and a mean of two shock episodes per patient when programmed in fixed tilt. So let's look at our results. First to look at first shock success. First shock success was better in the fixed pulse width group compared to the fixed tilt. Median success rates were 100% in the fixed pulse width group and 86% in the fixed tilt group, achieving statistical significance. There was a 14% intrapatient improvement in shock success when programmed fixed pulse width. 68% of our patients with fixed pulse width versus 45% of our patients with fixed tilt had 100% first shock success for all of their clinical episodes that occurred during the study. 78.6% of patients experienced greater or equal first shock success, and they did so despite slightly lower first shock energy. 33 joules versus 34 joules, which did not achieve statistical significance across the platform, but in intrapatient comparison, a 1.4 joule median energy difference. This is particularly important because one of the fears or concerns that people have from not using fixed pulse width is the fact that by its definition, less energy will be delivered. And when DFT testing is not done, there's been a potential concern leading to convention still being fixed tilt through now. Now let's look at patients who received first or second shock success. Again, fixed pulse width had improvement. The median in both groups was 100% of this IQR, but there were significant more patients in the fixed tilt who did not have success after first or second shock. As such, when intrapatient comparisons were performed, intrapatient shock success improved despite the overall population having 100% median success. 84% of patients with fixed pulse width versus 71% of patients with fixed tilt had 100% first or second shock success for all of their clinical events. 87.8% of patients experienced greater or equal first or second shock success, again here despite significantly lower shock energy. Shock energy did meet statistical significance here for a median of 33 joules versus 36 joules. And again, for intrapatient variability, 1.7 joule median energy difference of lower shock energy in the fixed pulse width. There are some limitations of our study. These patients were not randomized. Data was achieved from review of the Merlin.net database. Shocks were not independently adjudicated. We did not pull the clinical strips. The criteria for success was the device determining clinical success in return to sinus rhythm. The reason for reprogramming, which is obviously a concern we all have, is unknown to us. Why was somebody programmed from initially fixed tilt to becoming fixed pulse width? And why was somebody initially chosen as fixed pulse width and programmed to fixed tilt? This may potentially be due to whatever modality they were programmed first being unsuccessful, either with an unsuccessful shock needing a second or more shocks, or a dirty break that made the clinician uncomfortable in choosing to change things. This could have bias to the results. Neither the order nor the duration of reprogramming was randomized in our study. And long-term disease progression may have impacted shock success in either mode. What I mean by this is that patients were initially programmed to one modality and then at some point in their clinical experience were programmed to the second modality. This could lead to a bias in whatever second modality they had that by definition they are older and potentially sicker. Despite that, in our study, the majority of our patients, as I showed, 77%, started with fixed tilt and were programmed to fixed pulse width. As such, patients were older and potentially sicker in the fixed pulse width group. And despite this, the benefit was there for fixed pulse width. So for future directions, one can consider, based on this and other studies, initially programming fixed pulse width initially at the time of implant. Or just like we have devices that can switch direction of shock in first phase and second phase, starting with a reverse polarity for second or fourth shock or whatever, one can choose to this, to have the device recognize unsuccessful termination with first shock if the patient was programmed to fixed tilt, and then having the device automatically convert over to a fixed pulse width. This is not yet commercially available, but it's something we're working towards. So in conclusion, programming in patient-specific fixed pulse widths results in significantly greater first shock success compared to the conventional standard of fixed tilt waveforms in the same patients who've received shock therapies in both modalities. Thank you for your time. Any questions? Yes. Did you quantify the effect? I know you said it was a bias, but do you think there may be a correlation between the two populations? Potentially. If you look at the difference between the two populations, would it be appropriate to tilt? Since we're pulling the data from the Merlin database, not. What I'd like to do, though, at some point is we can identify, and for the paper, duration of time they were in one mode versus duration of time other, to see was it much later in life and such, because that data we can ascertain, but we haven't done that yet. That's for a deeper dive for the study, but that's a great question. Yes. So, in your data reports on first and second shock have all seemed to do away with and later shocks. Have you seen those? The question was whether we looked at later shock after first or second shock. We have not yet so far. The vast majority of patients, no surprise, do have success by second shock. But this isn't, by definition, a sicker population. These are patients who have received at least two clinical shocks. These are, whether they started out as primary prevention patients, they're far from that at this point. That's why, even with the two shock, we have lower success rates, even with second shock, in both modalities. It's specific to this population. But that's a great thought. We will try to do a little bit more dive towards that. Any other last questions? Because we're running a little bit behind. Thank you very much for your time. Thanks very much. And we'll move to the next presentation by Dr. Marco Schiavone. All right. Good morning, everyone, dear chairman, dear colleagues. I would like to thank the HRS for giving the opportunity to present the results of our study, which assess the role of the Praetorian score and defibrillation testing for assessment of the conversion failure in patients with the SACDs. This was analysis of the iSUSI multicenter protocol. Those are my disclosures. So we all know that SACDs represent an established safe and effective alternative to transvenous system for preventing sudden cardiac death in patients without pacing indications. And unlike transvenous SACDs, SACDs rely on anatomical landmarks rather than fluoroscopic guidance leading to a greater variability in implant positioning. And this may impact shock efficacy during the long-term follow-up of these patients. This found 20 evidence supporting the safety of omitting defibrillation testing during SACD implantation, current guidelines still recommend EFT at the time of implant. So I would just to ask you, how many currently still perform defibrillation testing at the implantation? Raise your hands. All right. So most of you do not perform defibrillation testing at the time of SACD implantation. This is very important to analyze our results for all those that do not rely on defibrillation testing. So we know the reason why most of us do not still perform defibrillation testing at the SACD implantation is that DFT itself carries procedural risk and most of all offer probabilistic outcomes that may not always reflect the real world performance of these devices during the follow-up. Indeed, in the instance of the shock-induced VF, in addition to shock strength and shock timing, which may be linked to the outcomes of the implant of the device, we all know that the amount of myocardium in its vulnerable period also plays an important role in the shock outcome. And this is, I mean, independent on the outcomes of the implantation of the SACD. We all know that by several works, the most important was published by Yashima and colleagues in 2003, which highlighted how the different reclutation and the amount of myocardium in its vulnerable period playing this important role in the shock outcomes as we may see here. Therefore, we rely on the Praetorian score. We all know the Praetorian score is an imaging-based developed tool which is used to quantify the risk of conversion failure based on device positioning and patient anatomy. We all know that it is, I mean, it may be assessed either via chest X-ray or as we published three years ago, either intra-procedurally with the use of fluoroscopy. So this study evaluated the predictive value of the Praetorian score for defibrillation success in this large international SACD cohort from the ASUC registry, and the primary end point of this analysis was a composite of DFT failure plus ineffective shock during follow-up. I want to stress on this because this was the first study actually relying also on ineffective shocks during follow-up to analyze the impact of the Praetorian score. So we evaluated the Praetorian score, its individual components, BMI, and impedance, which were assessed in relation to the primary outcome. Raw curve analysis with the lungs test were used to evaluate the model performance. The ASUC registry is a physician-initiated multi-center international registry involving 22 public and private institutions across Europe and North America. So basically, the registry is composed by 1,698 patients, but we had granular data only, let's say, for 1,063 subjects, which composed the overall study cohort. Mean age of this patient was 52.6 years, 77% of patients were male, and the mean BMI was 26.2. The most frequent reason to implant an SACD was in primary prevention in 62.4% of patients, and the most frequent underlying substrate was ischemic cardiomyopathy in 37.4% of patients. So most SACDs implantations were performed using the two-incision technique in 91.4% of patients, and intermuscular placement of the device was the predominant device implantation method in 86.6%. This was very important, actually, because although the intermuscular approach substantially reduces the likelihood of generator malpositioning, it does not complete the eliminating. So this is very important that a very high percentage of these patients were implanted with this technique. Here we may see how the Praetorian score was distributed along the study groups. We may see, actually, how most patients of the study core were, let's say, very well implanted, because Step 1 Praetorian score, the first class, was composed by 71% of patients, 79.8% of patients had the generator on or posterior to the midline, and 83.3% of patients. So not, I mean, everyone, but most, let's say, if 86.6% had this intermuscular placement, 83.3% had the CAN with less than one generator with the Praetorian score Step 3. With logistic regression analysis for the primary endpoint, intermediate and high-risk Praetorian scores were independent predictors of the composite primary outcome, both for intermediate-risk patients and for high-risk patients. Interestingly, Step 1 of the Praetorian score, generator and position anterior to the midline Step 2, as well as high BMI and post-shock impedance, were associated with the primary combined outcome. Other clinical and procedural values failed to be associated with conversion failure. So, actually, we took those variables that were able to predict the primary outcome in our court, and we, I mean, analyzed the role of the different steps of the Praetorian score, and we evaluated if the single steps of the Praetorian score were able, less able or more able to predict the primary outcome more than all the three steps of the Praetorian score taken together. So, as you may see here from the yellow curve, we have the Step 1 of the Praetorian score, the orange curve, the Step 2 of the Praetorian score, or red curve, the Step 3 of the Praetorian score, while in the dashed black lines, we see the overall Praetorian score, which reached the higher and the better area under the curve with a 0.71. So, basically, there were no statistical differences among steps, but the most complete role in predicting DFT failure was reached by the overall Praetorian score. Then, we built a multivariable logistical regression model combining the Praetorian score and the other variables that were associated with logistical regression analysis to the primary endpoint, and when combined, Praetorian score, BMI, and the post-shock impedance at the fibrillation testing, the combined model yielded a significant higher area under the curve of 0.78. The differences in the AUC between the Praetorian score alone and the combined model was statistically significant at the long test, reaching a P of 0.0078. So the addition of the BMI and impedance meaningfully improves the model's ability to discriminate the fibrillation outcomes, and the threshold for the BMI was identified at 26.3, an impedance of 81 ohms. Of course, this study comes with several limitations. This is a registry-based study subject to potential confounding, and although we employed a multivariable modeling to adjust for clinical-relevant covariates, the residual confounders cannot be fully excluded. The primary endpoint, including ineffective shocks during follow-up, relies on accurate device interrogation and consistent data reporting across centers, and the true incidence of ineffective shocks may be, of course, underestimated. So in conclusion, we may say that a high Praetorian score, elevated BMI, and increased post-shock impedance are independent predictors of conversion failure, defined as DFT failure plus ineffective shocks during follow-up. The total Praetorian score is a more reliable discriminator of conversion failure than its individual components, and a multivariable model incorporating the Praetorian score, BMI, and impedance significantly improves the prediction of conversion failure, and therefore, our study expands upon previous research by including ineffective shocks during follow-up in the primary endpoint, rather than restricting analysis solely to intraprocedural DFT. Thank you for your attention. Thank you very much, and we move to the last talk by Dr. Alfonso Aranda-Hernandez. Okay. Thank you. I would like to thank the organization for inviting us to present this work about prediction of BTVF from human electrograms using shortened variability. So this work is a collaboration between Medtronic and Utrecht University Medical Center. Those are my disclosures. And STV, so shortened variability of repolarization, has been shown to be a promising parameter in the identification of individuals at risk of sudden cardiac death and ventricular arrhythmias. However, its evaluation during daily living remains still challenged and unexplored. So this study aims to assess novel automatic methods for measuring STV in cardiac devices during patient's daily activities. So there is plenty of evidence around the STV parameter, but some of the latest and more recent evidence is the one you see here on the left. The group of Smoczynska et al., they look into differences in STV between baseline for a group of patients having non-sustained BT and BT. And they observed differences were statistically significant between baseline and both non-sustained BT and BT. The more they saw that during BT the increase was higher than during non-sustained BT. Also they observed that the increase was happening like two minutes before the recording. And similar evidence is coming from another group in Belgium, from Amony et al., in which they look to a similar finding, but in that case they use only non-sustained BT and they look primarily to patients having both ischemic cardiomyopathy and dilated cardiomyopathy. So on the right upper plot is ischemic cardiomyopathy, they saw an increase before the arrhythmic event and also in the dilated cardiomyopathy in the right bottom plot. In their case the increase was happening like five minutes before the event. So in our case we wanted to look for similar findings and for that we used the Medtronic Data Workhouse, so where we have EGMs associated to our devices and those EGMs are associated with baseline transmissions or event transmissions. So the scheduled transmissions are the baseline, when there is an event is the one we will use for the event. This kind of patients were basically ICD and CRTD devices primarily under guideline indications and we measured STB in both baseline and event transmissions and then we conducted a statistical analysis on both groups. So to calculate STB we have first to determine the QT interval and we already have an algorithm that has been extensively validated in human and animal models. So we use this algorithm to get QT interval, then we correct it for heart rate using Bassett correction and then we calculated STB as you see here. Our database initially was composed by 324 MBT and 60 PBTBF events, however we had to discard quite a lot of events due to pacing and also their condition like AF, SBT, abnormal depolarizations like PBCs, PACs and so on. Also some of the recordings didn't have a baseline and also no onset, so we didn't have EGM before the onset to be able to calculate STB properly. The median time between the baseline and the event was 98 days. Also another important factor when we are measuring STB is to correct or to control for confounding. So there are factors in the EGM signal that might increase STB values and are not linked to an increased risk for arrhythmias and one of those confounding factors are abnormal depolarizations. So in that case what we did is we discarded the bit before an abnormal depolarization, PBC or PAC and also two bits after that. Another confounding factor is noise as you see on the picture on the right, the purple line is the noise and you see how when the noise is increasing also is increasing the STB. So in that case we developed automatic algorithms to detect noise and we discarded those segments in the recording where the noise was above some predefined threshold. It's important to notice that here we did everything automatically with algorithms and AI to avoid any kind of human confounding while doing the annotations. Therefore when we have the, for example on the left you have the STB, the blue line, so we computed the average value on the recording and this is what we use for comparison between baseline and events. And on the right plot you see the point carrier plot, grey dots are the baseline, the blue dots are the event, so you can see that there is a higher dispersion in the blue points and this is what STB is measuring, this kind of dispersion in the point carrier plot. This is another example, in that case the heart rate during the event is lower than at baseline. So the results, so we saw that there were a significant increase between baseline and arrhythmic events in STB. On the right plot you see green lines is patients having increased and red lines are patients having decreased, so against what we were expecting. But overall differences were significant between those patients. Also if we now split the population and we look to MBT versus PBT-BF, we saw that increase even though in that case there were not statistically significant differences due to the low numbers on our population, but we saw that the increase in PBT-BF was higher than MBT and this is also in alignment with prior research in which they link the increase on STB to the severity of the arrhythmia, so higher increases are associated with higher severity in arrhythmic events. The limitations in our study are that we had a high prevalence of pacing, mainly due to our CRTD population, so we had to discard a lot of recordings and therefore we have a limited sample size that might potentially affect the statistical power of our results. Also we were not able to see where the increase was happening on STB. Prior authors, they saw it was between five to two minutes before the event, but we didn't have that much time before the event, so we didn't see where the increase was happening and that's a limitation. So as conclusion, so we validated that as prior literature that there is an increase on STB before the arrhythmia, so this has the potential to be like a clinical tool for evaluating arrhythmic risk and guiding patient management and while we saw this statistically significant increase, we didn't know or we don't know where the increase was happening and how much in advance we can get this increase to apply or make a corrective action in patients. So therefore as a future research, we aim to have this embedded in a device and try to do a prospective clinical study and validate those results. Thank you very much, I will take any questions you might have. Yeah, we have in the cobalt chrome devices, we have the capability to get a bit more left in the recording prior to the arrhythmia, so we use this, but this is cumbersome, it's not like available in Kerling, so it's something that is cumbersome to get this data and go through that. But in those devices, we were able to get close to 100 seconds before the arrhythmia. Sorry the question was about whether we have in the devices the capability to get enough length before the arrhythmia even. The question is about the algorithm, whether it's able to calculate the QT time in the EGM and which vector we use. So the algorithm is able to calculate QT from the EGM, and the good thing of the algorithm is it doesn't matter whether you have a biphasic T wave or normal T wave, so it's based on area and the absolute value of the area, and then we can determine pretty, at least consistently, what is the T wave and about the vector. We have done animal studies and human studies on what is the right vector, and it doesn't matter at all the vector. So the important thing is having a big enough T wave. If you have a small T wave, then you will have a lot of changes just because you don't have resolution to get enough accuracy. But the vector is initially not that important, I guess it might be important if the vector is capturing or close to the substrate where you have the arrhythmia, okay, I think this might be important. But in our findings, to have a good calculation of STV is more the amplitude on the T wave than the vector. Okay, thank you.

ICD technology

EVICD implantation

pediatric patients

MADIT-ICD benefit score

risk stratification

programmable pulse width

shock efficacy

Praetorian score

subcutaneous ICDs

repolarization variability