Good afternoon. We're going to get started. I'd like to welcome you all to the adult congenital heart disease oral abstracts. My name is Anna Camp and I am in charge of leading us through this great session. We have some really great science being presented today and without further ado, we have a very tight timeline. So we're going to start with our first speaker. I'd like to introduce Dr. Chung Cheh-Mao and he will present his data, Improved Survival with NOAC compared to VKA for Preventing Stroke in Atrial Fibrillation in Adult Congenital Heart Disease, Insights from the TRINETX database. Good afternoon, ladies and gentlemen. I'm Dr. Chung Cheh-Mao from Taiwan, Taichung Veteran General Hospital. I'm a pediatric cardiologist and also an EP. Thanks for the invitation from HIS, I'm glad to have this opportunity to share my study about NOAC versus Warfarin for Preventing Stroke in Atrial Fibrillation with ACHD. This is a real world study leveraging a large international data set to answer an important clinical question in a growing adult CHD population. Let me walk you through my study. Adults with ACHD face a markedly increased risk of stroke comparing to general population as shown from Swedish research, the stroke risk is significantly higher when aging. More than nearly all of these strokes are ischemic in origin with an embolic component suspected in more than 80%. This strongly underscores the need of effective anticoagulation strategy in this population. From the clinical guideline of stroke prevention in ACHD patients with atrial fibrillation, besides using Charles Vosgold to decide whether to use anticoagulation as a general population, there are two additional criteria. First, moderate or severe complexity of congenital heart disease. Second, age of more than 40 years. So how to choose NOAC versus Warfarin in adult congenital heart with atrial fibrillation from the 2014 PACE guideline and the review article from Canadian Journal of Cardiology. My complexity, ACHD with Charles Vosgold more than two, NOAC is better than Warfarin. In moderate to severe adult CHD, Warfarin or NOAC can be used, but NOAC should be used with caution. So what is the evidence supporting which type of oral anticoagulation in this population? The truth is no, due to their lack of randomized control trial in this special population. The only way to evaluate NOAC versus Warfarin use in this population can only rely on real world data. From the largest German insurance data, they enrolled 6,500 adult congenital heart patients using OCA, OAC. Surprisingly, patients using NOAC have higher all-cause mortality, MACE events, and bleeding than those who use Warfarin according to a multivariate analysis. Even they use propensity score matching, the NOAC have higher bleeding, tromboembolism, MACE, and all-cause mortality. So our study aim is simple but clinical relevant. To evaluate the clinical outcome of NOAC versus Warfarin use for stroke prevention in this population, we hypothesized that NOAC would have at least as safe or possibly more effective than Warfarin in this special population. This is a retrospective real world cohort study using Chinex Global Research Network. We identified adult CHT patient with atrial fibrillation who were newly prescribed either a NOAC or Warfarin. The baseline co-morbidity labs and medications were analyzed within 12 months of the index prescription. We excreted patients with mixed therapy and used one-to-one propensity score matching to balance the cohort. The primary outcome include mortality, bleeding, tromboembolism, ICU admission, and hospitalization. After propensity score matching, each group had around 18,000 patients with well-balanced distribution across different variables. The mean age starting for NOAC was 67 years old. The mean age at the end of follow-up was 72 years old. Latino are more and Caucasian are comprised for 80 percent. Comorbidity including the criteria in their CHBA score are also well-balanced. Also the medication of heart failure, hypertension, anti-aryxmic drugs, anti-polylet were well-balanced in two groups. Moreover, the lab data of anti-proBNP and LDL were also balanced. So here is the headline result. All-cause mortality was significantly lower in the NOAC group compared to Warfarin with a hazard ratio of 0.65. That is a 35 percent risk reduction. We also do their survival, this survival benefit persists across all their ACHE complexity level with the strongest effect observed in mild and moderate lesions. This is a major finding support the safety of NOAC beyond just stroke prevention. When we look at the major adverse cardiovascular events, there was a trend favoring NOAC, though their overall P value did not reach their significance. Composite hemorrhagic and thromboembolic and free survival was even higher in NOAC group. And here we can see the major bleeding survival. NOAC showed a significant advantage with a hazard ratio of 0.66. Reducing the bleeding risk is essentially critical in this fragile population. And then we stratified the ACHE complexity. The benefit of NOAC is reducing major bleeding persist, especially in mild and moderate ACHE groups. Although the severe ACHE subgroup shows a similar trend but did not reach the statistical significance. Intracranial bleeding, one of the most devastating complications of anticoagulation was significantly lower in NOAC group, had a hazard ratio of 0.67. Major thromboembolic events were also lower with NOAC. These findings are especially important because they challenge the historical reluctance to use NOAC in this complex congenital anatomy. Interestingly, the difference become more apparent in severe ACHD when NOAC significantly reduced thromboembolic event compared to Warfarin. In addition to mortality and bleeding, NOAC use are associated with reduced all cost hospitalization and ICU stay. And this real world healthcare utilization metric speaks to a broader system level benefit of NOAC, not just for patients but for institution health system. To summarize, compared with Warfarin, NOAC reduced all cost mortality by 35%. There was a 7% reduction of composite rate of hemorrhage and thromboembolic event with NOAC. When focusing on specific bleeding outcome, NOAC achieved 33% reduction in ICH and 34% reduction in major bleeding. And also the major thromboembolic event for 10%. Even the hospitalization and ICU stay also reduced. Ladies and gentlemen, to conclude my study, in this large real world study of adult congenital heart disease patient with atrial fibrillation, we found that NOAC was associated with significant better outcome compared to Warfarin. Specifically, NOAC use resulted in reduced all cost mortality, lower rate of major hemorrhagic thromboembolic event, fewer ICU admission, and fewer all cost hospitalization. Importantly, across all level of CHC complexity, mild, moderate, and severe, NOAC consistent shows a survival advantage over Warfarin. These findings strongly support the preferential use of NOAC for stroke prevention in adult with congenital heart disease and atrial fibrillation. Thank you for your attention. I would like to take any question. Could you tell us a little bit about the database that you used? You said it was an international database? Yes. The database we used is Trinex. It's actually mostly the, there are hundreds of center that upload their electronic medical record and including ICD code and procedure code and we can use that software to set some stratify, find our interest group and set the outcome and so we can just do it on the internet to find our cohort and compare the survival curve. So most of the center are from America and some of them from Europe and also some Asia. But I think most of them are from America, the medical institute. Are there any other questions for Dr. Chemal? Thank you so much, appreciate it. We will move on to our second speaker, Anushka Desai is going to present her data, Complications of Catheter Ablation of Atrial Arrhythmias in Adults with Congenital Heart Disease, a National Analysis. Hi everyone. My name is Anushka Desai and I'm a fourth year medical student at Georgetown University. Today I'll be presenting on the complications of catheter ablation of atrial arrhythmias in adults with congenital heart disease using a national database. I have no financial disclosures. As you know, the population of adults with congenital heart disease has been growing over the years due to advances in pediatric cardiology and improvements in cardiac surgery. With more of these patients surviving into adulthood, cardiac complications like arrhythmias are becoming increasingly common in this cohort. Atrial arrhythmias specifically have been known to be present in adults with congenital heart disease with a reported prevalence of around 15% and estimates of 50% in patients with severe adult congenital heart disease by age 65. The high occurrence of arrhythmias in these patients is a combined result of congenital abnormalities in the conduction system and structural issues leading to cardiac remodeling. In terms of treatment for acute settings, rate control is often difficult to achieve in atrial arrhythmias for these patients and even after escalation to cardioversion, these arrhythmias have a reported recurrence of up to 50 to 70%. These patients also often fail rhythm control with antiarrhythmics and are unable to tolerate the long-term use given their extensive side effect profile, leaving catheter ablation as the therapy of choice. Prior studies have shown that catheter ablation is associated with higher complication rates in patients with structural heart disease, but the safety profile of catheter ablation of atrial tachyarrhythmias in adults with congenital heart disease specifically remains unclear. We wanted to investigate this further by looking at the short-term in-hospital outcomes of this group. So, to do this, we used years 2016 through 2021 of the Healthcare Cost and Utilization Project's National Inpatient Sample Database, which is the largest publicly available administrative database in the United States. It contains hospitalization data from a stratified 20% sample from over a thousand hospitals across the country. Our cohort of interest was hospitalizations involving catheter ablation for atrial arrhythmias, namely AFib, AFlutter, and atrial tachycardia, and we divided this cohort based on whether they received, based on whether they had congenital heart disease or not. For our primary outcome, we looked at in-hospital mortality as well as secondary outcomes of post-procedure MI, stroke, and cardiac arrest. We also looked at various ablation-related complications, like access site complications, need for cardioversion, pacemaker, or cardiac surgery, and pericardial complications. Starting with a cohort of all admissions involving catheter ablation, we excluded pediatric hospitalizations as well as hospitalizations for which age, mortality, and procedure use data was unavailable. We also excluded hospitalizations that had co-occurring ventricular arrhythmias because we could not determine what the primary indication for ablation was for these patients. Our final study cohort included close to 343,000 weighted hospitalizations. For baseline characteristics, we used chi-squared and t-tests for categorical and continuous variables respectively, and for clinical outcomes, we ran multivariable logistic regressions adjusting for baseline demographics and cardiovascular comorbidities, which we selected based on a prior literature review. So when we characterized our cohort, we found that adults with congenital heart disease undergoing ablation were, on average, younger than those without. This is likely because congenital heart disease patients are known to develop arrhythmias at younger ages, given that they have a longer-term sequelae of congenital defects and prior surgeries. Most of the patients undergoing ablation were white, with more of the congenital heart disease patients having private insurance, being treated at larger hospitals, and having longer and more costly lengths of stay, likely in the context of their chronic medical conditions and the facilities required to manage complex cases. In terms of cardiovascular comorbidities, those who did not have congenital heart disease had higher rates of hypertension, diabetes, hyperlipidemia, chronic kidney disease, heart failure, and coronary artery disease than those with congenital heart disease. This is consistent with the general population, with these conditions being more prevalent and serving as risk factors for developing arrhythmias. In contrast, the patients with congenital heart disease develop arrhythmias more as a consequence of their congenital defect and surgical history, as opposed to their comorbidity burden. Here we present frequencies and adjusted odds ratios of in-hospital outcomes and complications following catheter ablation for atrial arrhythmias. For both adults with and without congenital heart disease, the most common complication during hospitalization was respiratory failure, followed by MI, and then pericardial complications. Those with congenital heart disease had significantly higher rates of in-hospital mortality, as well as stroke, cardiac arrest, pericardial complications, acute heart failure, and respiratory failure. And the adjusted odds ratios for these complications remained high as well, even after accounting for baseline characteristics and cardiovascular comorbidities. Even though in-hospital mortality rates remained relatively low, at less than 2% for both cohorts, those with congenital heart disease did have around double the risk of post-procedure mortality than those without. And this is likely explained by the higher frequencies and odds of stroke and cardiac arrest, as well as the need for subsequent high-risk procedures like cardiac surgery seen in these patients. The non-congenital heart disease group, however, did have higher rates of post-procedure MI, likely due to the higher prevalence of coronary artery disease and other cardiovascular comorbidities in this population. These conditions increased the risk of coronary events post-ablation, as the ablation sites are often close in proximity to the coronary vessels. All of these findings should be interpreted in the context of several limitations. First, the study is retrospective and cannot exclude confounding. For example, the decision of type of ablation used is dependent on the provider and their preferences as well as the hospitalization, as well as the hospital that the patient is being treated at. The National Inpatient Sample Database also uses data from single hospitalizations, which prevents us from looking at longer-term mortality, and the data is also administrative in nature and does not contain information on lab or hemodynamic markers, making it impossible to characterize procedural risk beforehand. And given that the database was based off of ICD-10 coding, we were not able to differentiate congenital heart disease complexity as well as between repaired, palliated, or unrepaired congenital heart disease. And the lack of procedural data also limited our understanding of patient-specific variations in cardiac anatomy that may have contributed to increased procedural difficulty and complications later on. There's also the risk of classification error where providers may drop the congenital heart disease ICD-10 code as an active diagnosis for the ones who undergo successful repair. And the same is true for arrhythmia burden and severity whether they are paroxysmal, persistent, or permanent, as well as for procedural characteristics like ablation location and lesion size. We also did not know the exact cause of death, which could have been insightful in understanding the mortality difference that we saw in congenital heart disease patients. And lastly, as I mentioned before, we did not have post-discharge outcomes and we were not able to evaluate the long-term risks that ablation may have in this cohort. Okay. In terms of main takeaways, we found that in our retrospective cohort, congenital heart disease patients had lower cardiovascular comorbidity burden, but higher in hospital mortality and healthcare utilization following catheter ablation. These patients specifically had higher odds of post-ablation stroke, heart failure, cardioversion, cardiac surgery, suggesting that the presence of congenital heart disease is associated with an increased post-procedure complication rate. Based on our findings from observational data, there's a clear need for more investigation into the safety profile of catheter ablation for these patients to better optimize their post-procedure outcomes. In terms of future directions, it would be helpful to look at differences stratified by congenital heart disease type to provide more meaningful interpretations of the data. And prior studies have shown that atypical atrial macro reentry tachycardias are more common with increased complexity of congenital heart disease, whereas AFib is more common in those with simple congenital heart disease. So it would be worthwhile to also look at stratifying by type of atrial tachyarrhythmia, as well as to see if specific combinations of ablation locations and congenital heart disease drive the high complication rate. So to conclude, our study highlights the increased clinical risk associated with ablation for congenital heart disease and underscores the need for future research to refine risk stratification and to tailor procedural strategies in this population. Thank you. The question is, do you have data on center volumes and could you put that into the model to assess outcomes and complications? The database did include information on hospital bed size, but that was the only marker that I had for center volume. Thank you. Our next speaker will be Dr. Ihab Gantos, and he will be presenting his center's data characteristics of inducible polymorphic ventricular tachycardia in repaired tetralogy of fallot before transcatheter pulmonary valve replacement, a multicenter catapult TOF registry study. Good evening, everyone. Let's wait for the presentation to load. My name is Ihab Lantus. I'm another congenital heart disease fellow from UCLA. I have some interest in EP and NET. Today, I'm presenting the clinical and acrophysiological characteristics of inducible perimorphic ventricle, VT, and repair tetralogy of fallot. I'm pleased to announce that this presentation or this article has been accepted recently, and two days ago, in the JAC-EP journal. This is the QR code for those of you who want to look at the full data. I have nothing to disclose. As we all know, patients with repair tetralogy of fallot are at increased lifetime risk for monomorphic VT or sustained monomorphic VT and sudden cardiac death. And as Carey et al. in 2004 already showed us that EP studies with inducible sustained monomorphic VT and perimorphic VT carry a very grim prognostic value for these very important prognostic values for these patients. While we know that monomorphic VT is linked with abnormally conducting anatomical asthmathes post-repair, the electroanatomical characteristics of perimorphic VT are unclear. And this is in part at least because we have low incidence of perimorphic VT in these patients. So our study took the, is a sub-study of the ongoing what we call it the catapult TOF registry, which is a multi-center registry taking centers from northern, the northern America, the United States and Canada. All these patients that were with repair tetralogy of fallot with native right ventricular outflow tracts who were referred to go for transcatheter pulmonary valve replacement underwent invasive EP study, which included the characteristics of all anatomical asthmathes to be evaluated in this EPS. These studies include programmed stimulation with at least, from at least two places in the RV endocardium with and without isopryl, conduction velocities below half meter per second was considered as more slow conducting anatomical asthmathes, and catheter ablation was performed to interrupt all the skies. A new entity that we tried to characterize in this study was what we called transiently organized PVT or from now TOPVT, which we characterized as at least three beats of stable QRS morphology with no more than minimal changes in the axis and appearance in over 10 of the 12 leads of the ECG within three seconds of the programmed ventricular stimulation. This has to be confirmed by three of the authors of this article. An example of this, as you can see here in blue, these are four different patients who had the blue section is what we call TOPVT, which is the transiently organized polymorphic VT. The results from our study was index EPS studies was performed in 186 patients. The mean age of these patients was 40 years. Fifty-five percent of them were males. Sustained polymorphic VT was in use in 46 patients, 25 or 25 percent of the registry, and polymorphic VT patient, polymorphic VT was in use in 27 patients or 15 percent. Out of the patients with polymorphic VT, sustained polymorphic VT was in use on, was the only arrhythmia in 21 patients, and it was in combination with sustained monomorphic VT in six patients. Some interesting findings from Table 1 with comparing monomorphic VT to polymorphic VT, there was no difference in age between polymorphic VT and monomorphic VT, no difference in gender, and when looking at the operative history, some interesting findings, patients with polymorphic VT tend to be operated on in the newer era. Patients with polymorphic VT tend to have, to at least have the systemic 2PA shunt, and patients with polymorphic VT had more history of non-sustained VT in the evaluations before. Looking at the ECGs, there was no difference in the QRS length or the number or the amount of patients who have more QRS above 180 milliseconds. Looking at advanced imaging, patients, the ratio of RVE end-diastolic volume index to LV end-diastolic volume index was lower in patients with polymorphic VT, and when looking at the EP study, patients with polymorphic VT tend to have less skies with, as we would expect, the minimal isthmus velocity in patients with polymorphic VT was faster. Looking at patients with polymorphic VT compared to monomorphic VT, they tend to have the minimum coupling interval was shorter compared to monomorphic VT, and if we take a look only at patients with polymorphic VT, so looking at the 27 patients, 6 of them did not have any catheter ablation. They didn't have any sky to be interrupted on, and repeat EPS happened in 4 of these patients. Repeat EPS was done after the implantation of the valve, and one of these patients was found to have monomorphic VT, and he got the intervention of implanting an ICD. The patients with polymorphic VT who underwent catheter ablation, there were 21 patients. After the ablation, 13 patients underwent repeat EP study in the same procedure itself. Out of these 5, they still had polymorphic VT. This was the intervention on all the 21 patients. Repeat EP study happened in 9 of these patients with polymorphic VT induced in 3 patients. With 2 of them, one was discharged with ICD and one on amiodarone. We had, during the median follow-up of 15 months, there were no cardiac events in the whole population of patients who were with induced polymorphic VT. If we look at the new entity that we characterized, the TOPVT, at baseline, it was observed in about 60% of the patients. Post ablation, it was observed in about 25% of the patients, and at the repeat EP study at about 10% of the patients. What we found was TOPVT beats were significantly faster than those of patients with induced monomorphic VT. The finding of more than one anatomical isthmus was associated with greater number of beats from TOPVT, and it was, there was non-significant correlation between the TOPVT and the number of anatomical isthmus. Looking here at the median number of beats of TOPVT at baseline EPS declined significantly after catheter ablation. Another interesting finding was the greater number of TOPVT, TOP transiently organized beats, the less likelihood you have the ability to induce at polymorphic VT after ablation, as you can see here. In summary, patients with polymorphic VT demonstrated fewer conventional risk factors as I've shown in the table one for future arrhythmic events as compared to those with monomorphic VT. TOPVT is a new entity. It could not be perfectly classified as either rapid monomorphic VT or polymorphic VT. TOPVT was noted in about 60% of patients with polymorphic VT at baseline. TOPVT was associated with the presence of anatomical isthmus, and they were observed less frequently following catheter ablation. Unfortunately, the clinical significance of inducible polymorphic VT was indetermined in this study. Of course, we have only 15 months of follow-up, so we need more data, longer follow-up, more patients, and maybe in the future we will be able to show something of this. And I will conclude with the central figure of our paper. Thank you for listening, and I'm happy to have questions. I was going to ask one question, when you looked at the variables between monomorphic and the transcendingly organized polymorphic, I didn't see anything about left ventricular function or delayed enhancement on MRI, have you looked at that yet? We did look at that, I just, in this table I just put the significant stuff, but in the full table you have the full information and it's published in the data, in our data. There was no significant. Nothing? Okay, great job. Thank you. So our next speaker will be Dr. Jeremy Moore, presenting Association between Slowly Conducting Anatomical Isthmuses and Ventricular Tachycardia Inducibility in Tetralogy of Fallot. This is very stressful to do all of this up here, I just want to say. Thank you, Anna. Thanks to the abstract adjudicators. So one thing I'm just going to start off by saying is that I didn't actually do this study, it was done by Victor Waldman, so I'm here on his behalf, he was not able to make it to the conference. The title of the study is Association between Slowly Conducting Anatomical Isthmuses and Ventricular Tachycardia Inducibility in Tetralogy of Fallot. Like the last abstract, this is a sub-study of the ongoing Catapult Tetralogy of Fallot registry, and these are my disclosures. So the background here is that conduction velocity through well-described post-surgical anatomical isthmuses has been associated with either inducible or clinical sustained monomorphic VT. A very specific study from Capel and colleagues in 2017 showed that the velocity cut, and this is spoken about in the last presentation, but a conduction velocity of .5 meters per second appears to be a very good discriminator between those with inducible VT and those without. This was based on a two-center study with 74 patients, and they also, if you look at the control section on the right here, they had 12 patients with normal hearts where they looked at conduction velocity in the RV outflow tract, and they found that none of these healthy hearts had conduction velocities less than .5 meters per second. So in view of this, this conduction velocity has been taken as a really important discriminator for inducible VT. However, it's not been validated in another study and has not been subjected to real-world analysis. So our sub-study of the ongoing Catapult registry was to evaluate the validity of this in an external cohort. So the entry criteria, this has been discussed already too, but the entry criteria are age over 18 years, tetralogy of flow or related variant, a native right ventricular outflow tract, so anybody who had any kind of surgical valve, transcatheter valve, or conduit in the RV outflow tract was excluded from the registry, and all of these patients were referred for transcatheter pulmonary valve replacement, so they had some sort of RV dilation with pulmonary regurgitation that prompted that referral. We excluded patients then who didn't have, who had surgical operations in the outflow tract, history of prior VT ablation, and importantly, if they didn't have comprehensive three-dimensional mapping, they were not eligible for this sub-study. The data were collected between 2017 and 2024. We collected baseline clinical factors and electrophysiology study characteristics. Again, three-dimensional mapping was performed with conduction velocity calculation. Like the last presentation, we used program stimulation from two RV sites, the RV outflow tract and apex, up to triple extra stimuli, down to 180 milliseconds with and without isoproteranol. The important definitions have also been described already, but a slowly conducting anatomical isthmus is a conduction velocity less than half a meter per second in a established anatomical isthmus. Early repair is defined as surgery before 1980. Inducible VT was sustained more than, was defined as sustained more than 30 seconds and the anatomical isthmuses have been previously described, which are shown here. Isthmus one between the ventriculotomy and tricuspid annulus, two is between the ventriculotomy and pulmonary annulus, three is between the pulmonary annulus and VSD patch, and four between the VSD patch and the tricuspid annulus. The primary outcome was inducible sustained monomorphic VT. We looked at descriptive statistics such as sensitivity and specificity as well as the area under the curve for various different conduction velocity thresholds across these anatomical isthmuses. And then we developed, to predict inducible VT, we developed a multivariable model using logistic regression and from the univariable model we took candidate variables and put them into a final multivariable model and then used that, used the beta coefficients from that model to develop a risk score for inducible VT using clinical factors beyond just conduction velocity. Here's an example of conduction velocity calculation. You can see this patient, basically we measure across abnormal electrograms in an anatomical isthmus, so we have in this particular case a distance of 21 millimeters and a conduction time of 28 milliseconds, yielding a conduction velocity of 0.9 meters per second. And we also oftentimes look at these by propagation. So this is normal conduction velocity between the isthmus, between the pulmonary annulus and the VSD patch. This is one with actually preexisting conduction block. We have seen that on a few occasions. And finally, slow conduction through this same anatomical isthmus here. You can see it holds up for a second, not a second I guess, but it holds up briefly and then passes through. So this is the study results. So the final study population consisted of 162 patients out of the 180 catapult registry patients available at the time with sufficient 3D maps. The primary outcome was observed in 42 or 26% of patients who had inducible sustained monomorphic VT. These are the baseline characteristics. I think the big things here, the mean age was 39 years. We had about 16% of patients with atrial arrhythmia at baseline, 14% with non-sustained VT. Overall, the cure restoration was 150 milliseconds. And we had preserved RV and LV ejection fraction at baseline, 55% for the LV and 45% for the RV. This is just a chart showing the increasing proportion of patients with slowly conducting anatomical isthmuses as you go from those with no inducible ventricular arrhythmia to those with purely inducible monomorphic VT. And in this last cohort here, we have 70, I believe it was 79% of patients. I can't see this myself. 78.6% of patients with slowly conducting anatomical isthmuses with inducible VT. When we compare those with and without inducible monomorphic VT, the major differences are shown in this chart here. Patients with inducible monomorphic VT were older. There was a higher prevalence of patients with surgery before 1980. We had a longer delay from surgery in this cohort. There was a greater number of patients with history of atrial arrhythmia, 33% versus only 9.7%. And we had more non-sustained VT in this group. There was a wider cure restoration, 165 milliseconds versus 146 milliseconds. And lower RV ejection fraction was significantly lower than those with inducible monomorphic VT. And finally, the absolute values for RV and diastolic volume and RV and systolic volume were greater than those with inducible VT. This is not normalized. These are the absolute values. Those are the ones that stood out in the statistical analysis. So larger RVs basically. This is showing the proportion of anatomical isthmuses associated with SCI or slowly conducting properties. And this is most commonly seen in isthmus 3 between the pulmonary annulus and VSD patch. Overall, the area under the curve for SCI using the conventional value of 0.5 meters per second was 0.71 for inducible VT. So this was not perfect. The sensitivity was 79%, specificity was 64%. And it turns out by adjusting that conduction velocity threshold at different levels, 0.74 meters per second was actually a better discriminator of inducible VT than 0.5 meters per second. And this is just a graph showing the different cutoffs that we evaluated and the better discrimination for 0.74 meters per second in this external cohort. Finally, the multivariable model for predicting inducible VT is shown here. Certainly, SCI slowly conducting anatomical isthmuses made it to the multivariable model. But also age, history of atrial arrhythmia, history of non-sustained, sorry, history of sustained VT and cure restoration were all included in the multivariable model. And when you look at this model for predicting monomorphic VT, the AUC of the area under the curve is 0.85 as opposed to 0.71 for SCI alone. This is the risk score that was created. It has a very similar model AUC as the multivariable model. And so you can use this to calculate the risk of your patient having inducible VT. And this is just a summary slide showing the major study findings, which are the high prevalence of SCI for patients with sustained monomorphic VT, the cutoff values being better with 0.74 meters per second, and then the multivariable model using clinical factors to predict inducible VT does seem to improve the prediction. So limitations, this is an observational design. Primary outcome was inducible rather than clinical VT. We did not centrally adjudicate the maps for the conduction velocity calculations. And of course, this is a select cohort before transcatheter pulmonary valves as opposed to the general tetralogy of fallot population. But overall, we found that SCI, although good, was an imperfect marker of VT inducibility. It's likely that other EP properties related to RV pathology have an additive effect on the development of inducible and probably clinical VT. And the incorporation of a clinical risk score does provide additive value for the prediction of inducible VT. So this is all. I'd like to thank all the co-investigators, many of whom are here today, without which we would not be able to have produced these studies. Thank you. Questions for Dr. Moore? Do you think based on your findings, should we redefine slowly conducting anatomic isthmus? I think so, but I'm a little biased, obviously. No, I think it's hard to know how to interpret the data. I think every time we have a subpopulation, we're going to get slightly different values because we're looking at sort of a bell-shaped curve probably in terms of what the point estimates are. But I do think it could be that the cutoff here might be, suggested it might be a little higher than previously thought. Was the EP study standardized across all centers, the same EP study for all centers? Yeah, that's a really good question. So we have a protocol that's shared among all the centers. So overall there's a lot of, a very common approach to all these, but people are using different mapping systems, different kinds of catheters. Even some, a few centers were doing bipolar mapping with just the ablation catheter. So there's some variation in how we're making these measurements. But overall, I think overall pretty similar. Okay, thank you. We'll move on to our next speaker. We have Dr. Frédéric Sauchère. He will present his center's data, or France's data, Impact of Congenital Substrate 3D Imaging Reconstruction to Guide VT Catheter Ablation, the CORICA study. Thank you. Thank you very much. So it's my pleasure to present this CORICA study on behalf of my other co-investigators for my conflict of interest. And here is the study. So this study was designed to tell the impact of congenital substrate 3D imaging reconstruction to guide VT catheter ablation in patients with congenital heart disease. As you all know, monomorphic VT are frequent in repaired congenital heart disease patients. And this is a complex, they have complex underlying anatomies and substrates. And besides that, recurrences remain common after ablation because of this highly heterogeneous and complex substrates. And imaging has been shown to help with anatomy but also substrate identification in other settings. So we wanted to test whether imaging could help in patients with congenital heart disease. So the aim of the study was to assess the role of pre-procedural cardiac CT scan or MRI to predict potential VT isthmuses in congenital heart disease. It was a retrospective study conducted in five centers specialized in congenital heart disease. We included 40 patients with a CT scan or MRI performed before VT ablation, of course. And these images based on the CT scan or MRI were modeled and we obtained digital treatment that was created with a dedicated software from Inert Medical. The potential VT isthmuses were annotated within the software by a free EP blinding to ablation and also blinding to the other annotation. And then we compared at the end all these annotations and compared to what was found during the procedure. Here is some example there. So this is the way we could delineate some ablation, some virtual ablation, and the colors represent the different EP. But we were blinding to the other mark and to the lesion performed by the other observers. And then just at the end we enlightened them to compare where the ablation lesion were placed and we compared that to what was found during the EP procedure. In this case the three different observers drew the same ablation site. In this one only two of the three did complete and target the same area. Here are some examples. This was a patient with transposition of the great arteries with surgical arterial switch. And you see that there is a scar there post-surgery and this scar actually was responsible for the VT and it helps that way to identify where the substrate were. Even though we had the 12-line morphology, the VT was pretty fast so VT mapping would have been pretty difficult. Here is another example with a repair double outlet RV, referred for recurrent VT. This was a CT scan though and the color coded for wall thickness and you see the heterogeneity of wall thickness and potential isthmuses based on imaging and in this case on CT scan. And that was compared to what was found during the procedure. And during the procedure we didn't have these images. It was retrospective so it was blinding to the images because we didn't have the models. So our population we include as I mentioned 40 patients and we divided that into two groups. Group A which was Tetralogy of Fallot or Tetralogy of Fallot-like patients which was the main group. Of course this is the most frequent congenital disease responsible for VT. And also group B with all the other complex congenital diseases and it accounted for 17.5% of the population. In terms of imaging we had CT scans and we can have both imaging for some patients but we have CT scans in 17.5% of the patients but we really tried to get the iodine acquisition because it gave us an idea of the scar itself, not just the wall thinning. But we have this information and this kind of sequences only in 17.5% of the patients. So it was pretty limited and by having a higher rate of these sequences it can certainly help to get a better idea of the substrate and MRI in 45% of the patients. But once again unfortunately high resolution sequences only in 27% of the patients. So not the best kind of imaging we can have at present time and with the best spatial resolution. Anyway what we find is that and we compare the ablation set on imaging compared to what was identified and the VT substrate that was identified during the procedure. And in that way all VT substrate identified on imaging by at least two observers we could identify the substrate in 87.5% and the VT substrate can be identified on imaging at least with one observer so it was not ideal but meaning that it was visible at least on imaging in 92.5%. For three patients I will come back on that 7.5% we could not identify the substrate responsible for the VT based on imaging. Here are the three patients without VT substrate identified on imaging. Two had focal or micro entrant mechanism. One had a VT circuit near a tricuspid bioprosthetic valve in a patient with congenitally corrected transposition of the great arteries. This is the case here. And another patient had a VT arising from the inside of pulmonary infundibulum stent in a pulmonary atresia with ventricular septal defect so possibly stent possibly irritating the substrate underlying so we did not identify on imaging this circuit or this substrate in these two cases. And another patient who had a re-entrant mechanism near the tricuspid annulus but substrate was not seen on MDCT performed without lead contrast acquisition and this is one other thing. It was a right ventricle, systemic right ventricle but still worsening is not all and having all piece of information is important and this lead iodine sequence 8 minute acquisition after contrast injection helps you to better identify scar in those patients so this is something important. But on the other side we identified substrates that were not expected such as infarct actually post-surgery and this was the case of the right free wall there in this patient so it allows to better identify the substrate in some patients and with substrate you do not expect to have in this sort of congenital disease so at the end we had 55 VTS muscles identified during the procedure so live during the EP procedure and mapped and 61 on imaging which gives a sensitivity of 85.5% and a predictive positive value of 70% and the observatory effect accounted for a minimal proportion of the total variance while most of the variance was due to difference between patients and actually between substrates because they have different substrates. So to conclude ladies and gentlemen, 3D anatomical reconstruction using this inert software allows identification of potential VTS muscles in most of the congenital disease patients. There was a good inter-observatory reproducibility and this approach may certainly help pre-procedural ablation planning and the idea is to widespread, it's currently limited to very specific center with high experience and having this piece of information may help to get a bit more in centers with experience in ablation but less experience in congenital disease. It can be overcome with this kind of information and detail imaging is important to reliably identify VT substrate so having high resolution MRI sequences or light contrast acquisition with CT scan is very helpful to identify substrate before ablation. Thank you very much for your attention. Thank you. Do we have any questions for Dr. Sacher? Can you repeat the question? So the question was we had MRI or CT scan and did we use wall thinning? So we did not use only wall thinning. Yes, we did in those patients with CT scan. It works less well with MRI because of spatial resolution of MRI which is not so good. So we were using wall thinning in patients with CT scan but it was not present in all of them. In one of the patients we missed, actually we did use CT scan. We did not ablate sequences and we missed the scar. It was an RV, a systemic RV but still an RV so less sick than an LV. So compared to what we are used to in ischemic cardiomyopathy or other non-ischemic cardiomyopathy, wall thinning is working pretty well in LV, much less in RV actually because it's too thin. Maybe with new imaging modalities such as photocounting and this kind of thing with spatial resolution we'll have more information. But I think the key there is having all piece of information is important. Thank you to all of our speakers today. Congratulations on all of your work and thank you all.

adult congenital heart disease

NOAC vs Warfarin

stroke prevention

catheter ablation complications

ventricular tachycardia

tetralogy of Fallot

3D imaging

TRINETX data

in-hospital mortality