Society and How to Use Society. The main title of this joint symposium is Advancing Materialism Management and the Clinical Outcome Between East and the West. I'm Xian Chen from Taipei, Taiwan. My co-chair is Mark Iwell from Canada, British Columbia, and in this session we have four experts in materialism field. I will introduce the first people is Dr. Zong Hua Bo from Taiwan. He will be talking about the differential of the materialism using the external infusion. Dr. Zong, please. Thank you for the introduction and it's my pleasure to be here, invited by this joint symposium with Traharian Society. So my topic will be focused on the external versus radiofrequency ablation for targeting the left ventricular arrhythmia. So here is my, there is no disclosure. So as we know that the summit is a very complex regions which was bounded by the left ascending LAD and also circumferential coronary arteries, which was separated into two part by the GCV and AIV. However, that's the clinical difficulty for doing the epicardial ablation is that 30%, almost one third of the patient with the GCIV actually was above the coronary artery. So it's very easy to damage the coronary artery if we did the epicardial ablation through the venous system as well. And also there is a lot of a situation with the different angulation, which therefore we traditionally separate into the septal summit as well as the lateral summit will be very difficult for certain kind of the angles. So this is the publication from Santa Jerez using the epicardial approach of the majority from the epicardial approach from the percutaneous way. And actually it's given a very high failure rate and very limited successful rate. So and also increase the risk of complication right now. It's very usual to be adapted for the summit region. And what is the, why the summit region is not very easy because that the local ablation, the activation time is not reliable, especially if we only focus on the bipolar electrograms. A similar study also showing that from the Windex group also show that the QS pattern based on the unipolar was how the relatively poor sensitivity and also the specificity for the true successful ablation site. And also owing to the waveform propagation probably it also highlighted that the lesion could originate in decreasing site. So right now we always move to the anatomy approach is given some benefit of the ECG findings such as the abrupt V3 transitions. So and also given more understanding about the anatomy that gradually we always use the, consider that the LCC-RCC interlevial triangle as a vantage point to get the successful ablation. So comparing to the conventional radiofrequency ablation, we have several ways to solve just based on the radiofrequency ablation. So there is a lot of ways listed below, but we will not discuss about several issues that was not considered to be the radiofrequency ablation. So the first one is the dispersive page that we could increase. It means that probably we will increase the systemic resistance which leads to the difficulty of the energy to penetrate deeper inside. So the most important is that we try to decrease the impedance which will increase the tissue density and also increase the lesion size. So therefore sometimes we could also move the location of the patches. Just like this is the example with the stepwise try to reduce the baseline impedance. So based on this publication, they try to reduce the impedance from almost to 130 to 110 and given this kind of situation, we could get the additional successful for the majority of the cases with the unsuccessful ablation from the original site. So the next way is that we could use the low tonicity irrigants. So because we know that when we use the normal CNI as the irrigants, so it just created just like a solid cloud and it will prevent the energy to penetrate into the tissue. So once if we change the irrigant to the half CNI or sometimes we use the glucose water, it will put more energy to penetrate into the tissue and therefore we could increase the lesion size. So this is also a sample showing cartoon figures. However, that's even we try to have used the low tonicity irrigants previously, we also found that especially for the outflow trial arrhythmia, the majority comes from the less submissive regions and we found that we could get additional successful ablation for almost to be the half of the cases. But the main issue is that for those cases, even we get the initial acute successful ablations without complications, but we still get a higher recurrence during the long-term follow-up. So this is the publication from Penn's group showing that there is also some pitfalls when we use the traditional ablation settings. So they divided the patients into two groups. One is the prolonged radiofrequency ablation, which means that you could separate into two minutes, three minutes, or even longer. So I think this method just provided additional insights that time is matter and additional to the contact. But the most important thing is that it was associated with relatively better short-term clinical success. And no matter which kind of a situation that we have, this is the summary that a long time ago, we collaborated with several centers and also tried to show in with a very big table showing that where we get the first approaches. But as we know that right now that we approach to be the most important part because sometimes we could get, even we get the very early recording electrograms, we still cannot get success from the early slide. But probably we could get from the adjacent structures or into the nearby to the origins. Additional consideration is going to the, how we call it, the preferential conduction. So therefore, even that origin was deeper inside, probably that early activation site was still a little bit far away from the origin. So in this case, in this series, we found that actually the acute procedure success could only reach in almost to be 84% of the patients. But the most important thing is that during a long-term follow-up, still almost to be the 20% of the patient with recurrence. So it means that even we use the bipolar ablation or use different strategies, we still have a relatively high recurrence just based on the conventional ablation strategy. So this is also a summary of the overall long-term outcome for recurrence, 20% with recurrence, no matter you started from where to do the initial spot that you put down. So the most important thing is once if the patient received multiple-site ablation, so it means that you have the higher chance to get recurrence. So the next step is that we discuss about the L-co-ablation for especially focus on the ventricular arrhythmias surrounding the submissive regions. So this is the advantage is that usually it could be useful as the alternative ways are relatively easier because you only need to wiring the venous system, but sometimes need some technique. And the disadvantage is that it very depends on which kind of the vessel anatomy structures that you have. And if you use the arterial cells, you probably will create it like AV block, or sometimes you have the coronary artery damage. Or if you use the venous system, probably you will cause the dissection. Traditionally, it will be self-limited, but we still need to be worried about that. So the next issue is that sometimes even we use a wire to record the earliest sites that we still cannot get success from there because as we know that we have several septal branches sometimes have different communicating veins there. And sometimes they communicate with the different septal branches. And therefore, once if you injected the alcohol into one branch, it will drain to another. So you could not guarantee that you have the total seal of your venous system. The next issue is that you cannot control the extent of the infarct size. So therefore, and also it depends on a lot of scale. So sometimes it will be very time consuming. So this is the example showing that actually you could use the 2-2-2 microcaster to record it in addition to the guide wire. And you could also use the microcaster to record the earliest site and try to find out which branch that you could target. So this is also another published parietal that showing the advanced technique, not only for the summit region, but the following paper also show it could be used for the SCAR-VT. So use the double balloon technique. So it could be double balloon with the distal protection or the double balloon venous approach. So I would not like to go through very detail, but this is the very useful way sometimes with the communicating vein that the alcohol just drained to another branch. And it could help to have the very limited operation of the summit region. And you could appreciate that the wire of the lesion after alcohol ingestion. So this is an overall summary of the outcome for alcohol ingestion. The acute success rate is not as high as that radio frequency operation. The most important thing is that the one year VA recurrence is still high, almost accounting for 25% to 30%. So communication rate is also high, almost to be the 15%. But based on later publication, it seems it could be decreased once if you have more and more practice and also experience on that. So this is the final slide that I will just like to show in what we did right now, but with the collecting data, try to collect more data in the future. So we just try to consider if when we do the radio frequency ablation that we have the almost 30% recurrence. So whether we could get additional benefit from additional alcohol ingestion, just no matter you get a success or not, you just try to inject it to the same anatomic structures and just try to have the very good seal and see whether we could get a better long-term outcome. So in this retrospect study that is the collection, we have the 11 cases which was performed by radio frequency first, but seven with the partial effect. So we finally moved to the alcohol and two with success, but we still injected the alcohol due to that the patient have the recurrent pattern. So two with the failed ablation, so we moved to alcohol ingestion. But however, for additional 10, the majority probably will fail, receive failed ablation outside, but we have the eight get success, two with the partial effect. Finally, these two partial effect was moved to RF ablation with one success, but one still fail. So the overall success rate is relatively higher comparing with the conventional radio frequency ablation only and or based on the external ablation only. Of course, that the long-term follow-up up to one year that the long-term success rate is around 90, but we still try to collect more data to confirm these findings. So this is the last slide. Thank you very much for your attention. Thank you. I'd like to invite Dr. Lange up from University of Michigan. Great. So thanks to Heart Rhythm Society and Taiwan HRS, the moderators, for the opportunity to be here. So I was asked to speak about ablation or class 1c antirethromic drugs for treating drug refractory VT in structural heart disease in patients with an ICD implanted. Who, when, and why? So let's go back to the old CAST studies. So the CAST 1 trial was published in New England Journal of Medicine in 1991, randomized nearly 1,500 patients with frequent PVCs and non-sustained VT after myocardial infarction to either ankinide, flecainide, or mericazine versus placebo. Study was terminated early due to higher rates of both all-cause and arrhythmia-related mortality as well as non-fatal arrhythmias with both flecainide and ankinide. After this, CAST 2 was continued with just mericazine, and this was also terminated early after a signal of increased mortality in the first 14 days in the patients who were randomized to mericazine. So importantly, the patient population enrolled in both CAST 1 and CAST 2 were patients in whom drugs were used to suppress asymptomatic or mildly symptomatic PVCs and non-sustained VT after MI, not patients with ICDs and sustained monomorphic VT where the risk-benefit ratios of using medications to suppress arrhythmias are quite different. Because of the results of the CAST trials, however, many have extrapolated concerns about proarrhythmia to populations that were not studied in those trials. And as such, there's been concern for using these medications in patients with structural heart disease. So what do the current guidelines recommend? The 2017 Guideline for Management of Ventricular Arrhythmias and Sudden Death gives 1C agents a Class 3 recommendation in patients with prior MI. Do not use in those patients. Meanwhile, for patients with VT and non-ischemic cardiomyopathy, there's no mention of 1C agents. Overall, beta blockers, amiodarone, sodalol, and VT ablation are all Class 2A Level of Evidence B recommendations. The 2017 Guidelines also give a Class 3 recommendation to avoid 1C medications or amiodarone for prophylactic antiarrhythmic therapy in patients with significant adult congenital heart disease with asymptomatic ventricular arrhythmias. So this recommendation is based on a multi-center registry study from 1991, which included 579 patients, young patients, who were treated with ankinide or flecainide for SVT or VT, which demonstrated high rates of proarrhythmia, cardiac arrest, and death. Importantly, the majority of these patients in this series who had an adverse event had significant underlying congenital heart disease, often with systemic ventricular dysfunction. So importantly, 1C agents can have negative inotropic effects, and this can be a concern for patients who have low ejection fractions and heart failure. So this study from 1985 demonstrated significant acute increase in RA pressure, PA pressures, pulmonary capillary wedge pressures, with significant declines in both cardiac index and LV function immediately after administration of IV flecainide in patients. Similarly, a small series from 1980s demonstrated high incidence of decline in LV function and worsening of heart failure in patients with heart failure and reduced EF who were treated with oral flecainide for maintenance therapy. So there's been some subgroups of patients in whom Class 1C agents have shown to be quite effective. These are patients with channelopathy, such as LONQT3 and CPVT. Furthermore, it's been used as well in structural heart disease patients, such as those with ARVC and, more recently, arrhythmogenic myelodromic prolapse. One subset of patients with non-ischemic cardiomyopathy in whom flecainide has been documented to be quite effective and safe in suppressing ventricular arrhythmias is patients with arrhythmogenic right ventricular cardiomyopathy. And here's just two of the prior studies. And a more recent series in Jackie P, just published online, which enrolled 191 patients from 12 centers with ARVC, importantly, including 35% of whom who had LV involvement as well. Treated with flecainide, followed for a medium of over four years. There's reduction of PVC and VT episodes after flecainide use, and it was well tolerated, discontinued in only 8% of patients, 4% of whom had suspected proarrhythmia. More recently, it's been established that it could be beneficial in patients with mitral valve prolapse syndrome and mitral anterogist junction. This is a small case series of seven patients with symptomatic ventricular arrhythmias refractory to beta blockers who were treated with oral flecainide in whom arrhythmias were able to be suppressed effectively. There were no adverse effects in this small series. This study here was published by the Penn Group, relatively small study of 20 patients with frequent PVCs and suspected PVC-mediated cardiomyopathy who were treated with 1C agents. Most had undergone at least one prior ablation, and six of whom had a defibrillator or LifeVest in place. Mean PVC burden decreased from 36% down to 10%, and mean ejection fraction decreased or increased from 37% to 49% on flecainide. So this was a patient population with suspected PVC-mediated cardiomyopathy who were managed with flecainide effectively. There were no adverse events in this series. This more recent study from the same group examined safety and efficacy of 1C agents in patients with non-ischemic cardiopathies and ICDs in place. Again, a relatively small sample size, 34 patients are collected over an eight-year time period who were treated with flecainide or propafenone for symptomatic PVCs, the majority of whom had failed other anti-rheumatic drugs or ablation. PVC burden decreased from 20% down to 6%, and EF increased from 33% to 37% with no adverse events. So revisiting the title of this particular talk, ablation or class 1C anti-rheumatic drugs for treating drug refractory VT in structural heart disease and ICD implanted. Who, when, and why? So the 2019 VT ablation guidelines have recommendations for VT ablation in patients with both ischemic and non-ischemic cardiomyopathies. For patients with non-ischemic cardiomyopathies, there's a 1B recommendation for VT ablation in those who have recurrent VT refractory to or intolerant of anti-rheumatic drugs in preference to anti-rheumatic drug escalation, especially in the setting of VT storm. And then there's a 2A recommendation for ablation in patients who prefer not to be on anti-rheumatic drug. So a fairly strong recommendation to favor ablation. Furthermore, there have been several retrospective analyses examining the benefit of early VT ablation, which have all shown fairly similar results, suggesting significant reduction in VT recurrences and ICD shocks, but no statistically significant improvement in mortality at a cost of increased procedural and periprocedural complication rate. In 2022, the results of these three randomized control trials were published, the PARTITA study and SURVIVE-ET trials from Europe and the PAWS SED trial from Asia. PARTITA and PAWS importantly enrolled patients with non-ischemic cardiomyopathy, which is a subgroup of patients in whom 1C agents is likely to be considered. And SURVIVE-ET enrolled ischemic cardiomyopathy patients where they found that substrate-based ablation was superior to anti-rheumatic drugs as first-line therapy and associated with less adverse treatment-related effects. PARTITA showed that early VT ablation after first ICD shock improves mortality compared with conservative management and waiting for storm. And then PAWS SED showed that in patients with VT undergoing ICD implant, early VT ablation can be performed safely with low complication rates, even epicardial, and reduces VT recurrences in ICD therapies. More recently, results from the VANISH-II study, which randomized post-MI patients with VT to either ablation or anti-rheumatic drug with either amiodarone or Sotalol. Over 4.3 years follow-up, ablation showed superiority with regards to the primary composite endpoint. So to summarize, 1C agents should be avoided in patients with asymptomatic or mildly symptomatic PVCs and non-sustained VT in the setting of prior MI. This is the study group that the CAST studies enrolled and showed detriment. There's limited data on efficacy of 1C agents for VT in patients who are refractory to amiodarone or Sotalol. There's no large studies signaling harm when using 1C agents for VT in structural heart disease outside of post-MI patients or those with significant congenital heart disease. Be cautious of worsening heart failure and hemodynamic decline in patients with reduced LV function when using 1C agents. 1C agents may be especially effective in certain patient populations, such as those with arrhythmogenic cardiomyopathy or arrhythmic mitral valve prolapse syndrome. Evidence supporting catheter ablation as initial treatment option over anti-rheumatic drugs, including Sotalol and amiodarone, there's earlier ablation may be associated with improved long-term outcomes. However, 1C agents can be considered in non-ischemic cardiomyopathy patients with ICD, especially in those with continued arrhythmias refractory to ablation or in whom ablation is contraindicated or deferred. Thank you. Okay. Next speaker is from the Taiwan Heart Aid Society, Dr. Lin. You are talking about right-left metrical-metrical ablation, a stabilized approach. Thanks for introduction. I'm Dr. Lin. Thank you for introduction, I'm Dr. Jin-Yu Lim from Taipei, Taiwan. Today my talk is about RA to LOV, VT ablation and the stabilized approach and the clinical outcome. It's used in a common concept that when we do a VT ablation, usually we approach the VT from two ways. One is from the retrograde through the LV valve and anti-grade through the mitral valve. Or in some cases we can do the epicardial puncture to approach the epicardial axis to ablate the LV, VT. However in the patient with mechanical LV valve or mechanical valve, actually it's very easy to get entrapment and have broken to the mapping castor or ablation castor. There are several reports describe this kind of trauma during the mapping and the castor was broken and caused a surgery to open the heart and retrieve the castor in this kind of case. And also in the previous study, the professors or GMA used the epicardial puncture to do the mapping for this kind of VT with the mechanical valve. But in this kind of case can only approach the VT original from the apex, cannot approach for a patient with VT from the septum. And also there are several methodologies that use the direct apical puncture or surgery assist the trans-apical axis to do the ablation. However in this kind of surgery usually cause some severe bleeding in vein and also some complication and take times to recover by this kind of maneuver. So there are several other methodologies that we can use the RA to LV axis or interventricular transeptal axis to approach the left ventricle. Smaller interventricular transeptal approach have a thicker muscle in the ventricle and cause a more longer transeptal depth. So it may more favor to use the RA to LV axis. And this is the gross anatomy in this area. And then we can see that in this anatomy there is a, this is RA and this is LV. And we can see that below the membranous septum and anterior to the coronary sinus, there's a muscle layer which is thinner in this area, which connecting the right atrium to a LV ventricle. And this is a way that we might do the transeptal puncture with less tissue damage in this area. In the CT view, we can see also there is a thin muscle layer in the RA between the RA to LV. So it could be a way to approach the left ventricle in the patient with mechanical artery valve and the mechanical valve. And this is the preparation for this kind of procedure. Usually we need a general anesthesia and use the eyes and the fluoroscopic guide and the defibrillation and with inner 5-inch guiding catheter for this kind of approach. And usually we need eyes to accurate locate the area between the right atrium to the left ventricle. And we can use the abrasion wire or the needle to do the transeptal puncture. And this is a view that during the transeptal puncture from RA to LV. And then we can see that this is the RA view. And this is the defibrillation and this is the inner guiding catheter. And this is the RF wire. And the eyes is located in the low RA, a little bit lateral. And when we do the clockwise rotation, we can see this view. And this is during the wire abrasion and we can have a transeptal to this area. And this is the detail of the procedural step. The first one that we use eyes to locate the area of the transeptal site, use the flarable long shoes to manipulate and move the long shoes to this area. And we can start to do the eye abrasion in this area. And this is when we do the eye wire abrasion. And we can see the wire across the transeptal area to the LV ventricle. And after we put in the wire to the left ventricle, we can use the inner guiding shoes or micro catheter to change more stiff wire into the LV. And change it to the balloon to dilate the septum between the RA to LV. And this is used micro catheter to changing for stiff wire. And then we can have more support for the balloon to cross the RA and the LV. And this is during we dilate the balloon and dilate from RA to LV, then we can cross the flarable long shoes into the LV and complete the procedure. In some area that may not have eye wire, still not have eye wire, we can use the tail of the arteries shoes wire. And you can use the abrasion energy to assist the abrasion in this septum area. This is an example that we do with the arteries wire with the tail into the RA to LV area. And we use the cutting energy, 40 watt, which can easily transeptal into the LV. And then we can advance the guiding catheter and change it to a stiff wire. Then we can advance the balloon and dilate, then putting the flarable long shoes into the LV. This is in case that if the eye wire is not available. And this is the video showing that we use the tail of the arteries wire, and then we put in the guiding catheter into the LV and changing to a stiff wire, and then change back to the balloon and do the dilatation. Now, it should be very careful that because in our study cohort, and also in my experience, actually when we do the RA to LV puncture, actually can induce a very fast VT and even ventricular fibrillation during the procedure. So usually after the puncture, we need to do the defibrillation in this kind of case. In our cohort, we have a collaboration with many centers from USA and Europe, and there are totally 18 patients. And we can see that actually VF and VT occur in four and eight patients in this cohort. And all the procedure was guided by the eyes during the transeptal puncture. And if there is a VT or VF, we need to do the defibrillation. And we found that actually during the puncture, we induce a fast VT, and then when we do the pacemaking, actually this area is compatible with the transeptal area. When we do the pacemaking, the morphology is almost the same. And also there are some cases that during the transeptal puncture, actually the patient is under a VT before the transeptal. And in one case, the transeptal procedure terminate the VT. And finally, we found that actually the transeptal site is correlated with VT isthmus in this area. So the transeptal cause termination in this VT. And this is a multi-center study, and we collect 18 patients from 10 centers from United States, Europe, and also Asia, including our hospital. And all the patients have double mechanical valve. And for safety, actually during this 18 experience, there's no new AV block. And one patient demonstrated intramural hematoma at the transeptal site. And actually there's 10 patients have remaining LV to RA shunt after the procedure. But actually there is no decrease in the LV function or other complication in this patient. And currently the long-term outcome, three patients have experienced recurrence VT and also the ICD therapy. And also there are three patients actually died after in the follow-up of the procedure. And two was due to a VT recurrence, and the one is not due to a VT recurrence. And by this experience, we found that through our knowledge of anatomic relationship, and also the evidence of the ice guide and the fluoroscopic guide procedure, performing the catheter abrasion in patient with the mechanical valve and mechanical mitral valve could be safe. And actually good efficacy by this kind of way from RA to LV puncture. And actually we can do the mapping because the long-shoot transeptal from RA to LV actually is very stable or not easy to get in and out by this approach. And this maneuver is even better for mapping comparing to the RV to LV approach. And this is a more straightforward by this way rather than other methodologies like apical puncture or epicardial puncture. Because in this kind of maneuver, we have some limitation for mapping in some area of LV. But this kind of approach may need some experience for this technique because for my first approach, it take around 30 to 40 minutes to salivate transeptal to LV. And also my friend Pasquale also tell me that for a second time, the procedure time will be decreased a lot. So maybe in the future, in this kind of patient with mechanical valve and LV-VT, maybe we can use this kind of approach to safely and effectively to treat the VT ablation in this kind of patient. Thank you. I'd like to invite Dr. Zoua to talk to us from the University of Colorado about ablation and severe heart failure. Thank you. It's a pleasure to be here. I'm delighted to participate in this session. And I think the prior talks highlight how important it is and how complex VT ablation can be to involve all aspects of care. And so that's kind of going to be the focus of my topic. Sorry. So I'm going to talk about how to prepare and organize VT ablation in patients with severe heart failure. Disclosures were reviewed. So you know, VT ablations are not just complex procedures. They are a complex process. So what that means is that there are multiple teams that have to be involved, not just involved but actively participating and collaborating with one another in order for a success to be achieved. When that works well, what we demonstrated is that even in patients with severe heart failure, that the outcomes for those patients without recurrent VT could be quite good. In fact, in this study from the International VT Center Collaborative Group, which included more than 2,000 patients with structural heart disease undergoing VT ablation at multiple centers around the world, patients with the worst kind of heart failure, so New York Heart Association classification for who otherwise would have a terrible prognosis, could be rendered to have an almost equivalent outcome and survival to those patients with lesser degrees of heart failure. Humbling but true, and kind of highlights the very narrow therapeutic window for treatment and control of VT in these very frail patients, is that when we are not successful, either because VT recurs or other things happen in the case that make us limited in what we can do in the case, then the survival is clearly much worse. And those are the patients in whom we like to learn from to kind of improve outcomes moving forward. In most of these cases, I think that the key to success or failure is attention to maintaining hemodynamic stability. So this is data from the Penn Group, 193 consecutive patients, 22 or 11% of those patients had acute hemodynamic decompensation intra-procedurally. And while those patients were able to survive and even be discharged from the hospital in many cases, the downstream effects were lasting. So 50% mortality in those patients in whom acute hemodynamic decompensation occurred up to two years afterwards. And trying to rescue these patients, for instance, with rescue mechanical circulatory support or ECMO, is not really a thing, as it turns out. So again, the Penn data showed in this group of 21 patients for that practice of implementation of rescue ECMO, so, you know, they were already crashing and burning, and at the last minute we call in our CT surgical colleagues to help. What you can see is that over a median of 10 days, the majority of patients didn't even make it out of the hospital, and those that did clearly also had poorer outcomes as well. And the primary mechanism for failure was heart failure in most of these cases, again alluding to the fact that management of hemodynamics is critical in these patients. The Taiwanese group also showed a similar result with their cohort of patients in 81 patients undergoing ablation. Those in whom rescue mechanical circulatory support was required did significantly worse in terms of survival, typically because of heart failure. So how can we do a better job? How can we learn from these opportunities to optimize outcomes? What has become clear is this importance, and I'm going to stress it repeatedly, about maintaining hemodynamic stability. And this requires an active collaboration with our anesthesia teams as well as every staff member working in the lab. We minimize VT inductions when possible, focusing on substrate-based ablation. All of this helps to also optimize procedural time and efficiency, which have also been shown to improve outcomes. So anesthesia has truly become integrated into our practice, certainly here in the West. This joint session is about East versus West, but I think it's all the same around the world. So much so that this essential consensus document was published within Heart Rhythm last year talking about how to manage anesthesia issues that come up during EP cases. Dr. Santangeli and I were honored to write the VT ablation section. And really what I can't stress enough is how much we prepare for the worst. And one of the ways that we can do that is to anticipate risk. The Payne's d risk score, which is one of several risk scores that have been developed to predict acute hemodynamic decompensation, probably the easiest to use and therefore to validate. But you can see there are a number of clinical risk factors that each have a weighted risk for acute decompensation associated. And you can add up all the points and divide into tertiles of risk. And what you can see is that with the increasing tertiles of risk, you have a dose response effect essentially of causing acute hemodynamic decompensation, which I again emphasize in a different way. The mortality or survival is quite poor in those patients. Of these risk factors, the only thing that especially on the table that we have active control over is how the anesthesia is managed. And that part is critical. So whether we're using sedation or general anesthesia, and practice patterns are different not only around the world, but certainly within different sites within the United States, different agents that are used have different hemodynamic effects. Many of them will have negative inotropic effect and decreased cardiac output. Most of them have some impact of vasoplegia, which can cause hypotension. And it is really critical how that hypotension is managed. So these are the most common anesthesia agents that are used to combat hypotension. The top three are pure vasoconstrictors. What they do is they increase the work of the heart, especially in hearts that are weak. Now in hearts that are strong, normal, you know, and we have anesthesia providers of all different disciplines that kind of circulate through our lab. We're not always privileged or lucky to have a cardiac anesthesiologist support these cases. And unfortunately, you know, the go-to drugs that are typically used outside of the cardiac space are the top two, phenylephrine, ephedrine, very easy to dose, very comfortable for these providers to use, and they are very effective at increasing systemic vascular resistance, which especially in the vasoplegic phase of induction of general anesthesia can be important. Now in this space outside of the EP lab, outside of structural heart disease, these work just fine. There's no impact on cardiac output. The problem is they do nothing to support the heart. They are not, they don't help to augment contractility, and in the setting of compromised baseline reserve, they actually can reduce cardiac output and lead, this can trigger then this vicious cycle of hemodynamic collapse. The agents that follow that have beta agonism associated with them are far more effective to use in these patients with structural heart disease. They tend to increase cardiac output, and when paired with agents like inotropes, which decrease the work of the heart by decreasing the systemic vascular resistance, dobutamine in particular is a beta 1 agonist, they all can concomitantly, synergistically work to improve the cardiac output. So case in point, so this is a patient that was brought to our lab a few years ago, and what you can see on the echo image here is at baseline how very terrible the LVEF is. I will disclose here fully, and you can see it in the anesthesia record, this patient didn't even have VT. The patient had flutter with variable conduction. Shown here are the baseline blood pressure, the heart rate, noninvasively, then invasively. What's the first drug that's used to kind of augment or prevent vasoplegic hypotension in this patient? Of course, phenylephrine. Phenylephrine, why not? Well so this heart, this heart in particular, already working so hard, is now kind of freaking out because there's so much more work for it to do. And what happens is a sympathetic surge that then you can see the heart rate trend shoots up. Why? Because now they're in one-to-one flutter. What does that do to the blood pressure? Not good things. So then there's this series of hyperreactions, overreactions, especially in the context of induction of anesthesia where you get pops of epinephrine, pops of phenylephrine, an increase in the baseline phenylephrine dose, which then paradoxically causes this like hypertensive emergency situation where they institute nicartapine to try to bring the blood pressure down, a calcium channel blocker in a patient with heart failure. That's crazy. So it's only when we start to implement drugs like epinephrine, dobutamine, that we start to get some relative stabilization. But it's kind of fake, right? So this is an average. But you can see that moment-to-moment there's a huge amount of stress and adjustments that are being made to try to temporize this patient, to try to prevent them from dying on the table. We even try to cardiovert, get them in the sinus rhythm. We're thinking that that will help. It's only after the realization that the phenylephrine is still going and we stop it that we actually see stabilization that's real. And in fact, a hemodynamic improvement that rivals how the patient was at the beginning of the case. And we haven't even done anything with the patient yet besides cardiovert them. So we studied this at our institution, looking at vasopressor choice related to outcomes and looking at the use of only afterloading increasing agents and impact on patients with severe heart failure. And you can see there's the same dose response effect that leads to worse outcomes. Outcomes defined as 90-day mortality, so death within three months when these agents are used in these cases. And when it's just a single agent that's used, there's a cumulative dose effect that goes in the same direction. So there are data to support this risk prediction to also advocate for preemptive mechanical circulatory support. These are two studies that kind of highlight this. Both comparable patients with structural heart disease and VT. You can see that the pains D scores in each of these studies was fairly equivalent. But what is different is that those in whom empiric or prophylactic percutaneous LVAD support was provided did significantly better in terms of acute decompensation. And that tracked with 30-day mortality. And again, the point that when you try to rescue these patients, it's too late by the time they've decompensated. So a very huge other point is that we have to constantly remain vigilant about not wasting time. Because time can make the difference in survival. This is data from UCLA, 148 patients undergoing substrate-based ablation with the procedure duration defined as time from vascular access. We haven't actually gotten in and mapped anything yet. It's just putting the sheaths in and time to sheath removal. But they clearly showed, and people who work with me know this, after six hours, the outcomes are much worse. People die in the hospital more frequently when the procedures for VT ablation extend beyond six hours. Now there are obviously other factors that go into this. Inability to control the VT, placement of a balloon pump. But regardless of what the baseline covariates are, or baseline comorbidities, as well as the intraoperative characteristics, that six-hour time point remains important. So in my lab at University of Colorado, we work very hard to try to stay below that threshold knowing that this is the potential outcome. So catheter ablation is an effective treatment. It can be used to help and even improve survival in patients with heart failure. But the key thing is that we have to prevent acute hemodynamic failure. This involves our active participation in how the hypotension in these patients is managed. With preference for use of beta-1 agonists, inotropes when possible, avoiding afterload increasing agents, considering mechanical circulatory support in high-risk patients. This obviously involves the active involvement of the heart failure service, cardiothoracic surgery, and multidisciplinary input. And time is safety. We all have to be very stringent and systematic about ourselves and teaching our staff and our fellows, who are the future of our profession, to use it wisely. I will thank you and take any questions. We'll get the speakers to come up for questions. You can either join us and ask a question on the microphone, or you can use the QR code to jump in. Hi. I'm Cristiano from Brazil. I have a question for Dr. Liang. In the past, we have a lot of Chagas disease there in Brazil. And in the past, the device clinic guys used a lot of propafenone in Chagas, and could see very slow VT below the ICD detection. And do you think it's specific for Chagas, or we must be aware? Because we can see on the ATRA, the ATO1C flutter, do you think for other cardiomyopathies, this is also a problem? So I'll be honest with you. We don't have a lot of Chagas in Michigan, so I do not take care of a lot of Chagas patients. I would say that with any anti-rheumatic drug, with any scar-related VT, introduction of anti-rheumatic drugs can alter the conduction properties in slow VT. We actually examined that effect with quinidine for monomorphic VT in structural heart disease, and found that a lot of our patients that we treated with quinidine had a similar result, where the VTs now became slower than the therapy zones. So definitely something to keep in mind. It certainly can happen with propafenone. Thank you. Can I ask a question? Yeah, sure. I guess. Sorry. Along those lines, I really loved what you presented, because I think the messaging for flecainide and 1C agents has really extended beyond that ischemic group, which is really what was studied. Dr. Presani brings up a good point, too, about any kind of scar-based disease. I believe in the Penn cohort, that included patients who had LGE on MRI, and it was still found to be relatively effective, at least at PVC suppression. That's probably different than the VT group. But I think that any anti-rhythmic, though, can do that, can slow VT and make it more difficult and incessant. Great talk from everybody. Dr. Zil, do you think you can avoid the negatives to GA by prophylactically giving inotropes? I started using GA all the time on my VT ablations, just patients not moving, everything stays stable. But I wonder if you redo the pain set score now and prophylactically use inotropes up front. Do you think you can bypass that? That's a great question, a great thing to study. We do do that. Before we start, we do things to try to buff up the blood pressure. And then that's more specific to when we think we're going to try to induce. Again, I said that we try to minimize inductions, but that's still included as part of the end point for ablation, and sometimes the starting point if we don't have a template, you know, a 12-lead. But I think that that is important. We do a timeout at the beginning with anesthesia, and throughout the case, I'm asking, did you use anything for blood pressure support? What are they on for pressers? And I think that that helps. Please. Yeah. One thing I wanted to point out, too, is, you know, some of the studies that Dr. Zoh showed with the hemodynamic support, those were published in 2018 and 2019. And this was back when people were doing point-by-point mapping with the ablation catheter, repeated inductions, before the HD grid, before the optrol catheter were being used, and all these substrate-based ablation approaches. So just keep that in mind. There was a more recent series from the Cleveland Clinic Group where they did the 5-0 impella, and it actually did not show benefit, similar to those other series. Great discussion. Thank you. A question for Dr. Liang. For hypertrophic cardiomyopathy, was your approach with these patients for class 1C still structured disease, and would that change if they had a septal magnetomy or they have already ICD? How would you? Yeah, so that's a good question. There's actually been data, I think from a Japanese group, where they looked at flecainide and its negative inotropic effects on hypertrophic cardiomyopathy, and it was able to be used safely to almost similar to disopiramide as a negative inotrope in hypertrophic patients. My general approach is to ablate these patients. And if ablation fails, if we're not able to eliminate VT with ablation, then certainly flecainide would be considered. It wouldn't be my first choice, but I would not offer it. And this issue comes up a lot with atrial fibrillation. Patients with AFib who have 1.7 or 2-millimeter septum, is it safe to use flecainide or buprenorphine? We have used flecainide in those patients, even without ICDs, and they've done well. I might take the prerogative and ask Dr. Chung a question. Just about workflow, in terms of considering ethanol ablation and patient selection, are you planning on using it, sort of preparing to use it up front based on the patient's ECG that they come in with, or are you predominantly doing this in a staged procedure, trying RF first, and then bringing them back for a second procedure? Because that's, of course, we could try first shot for, because our radio frequency and also our mapping is relatively easier, so we could prepare the alcohol ingestion as the next step, but that is, given the data that we show from the multi-center collaboration, we found almost 40 percent, if you count in for a failed procedure, and also those cases with recurrence, it's accounting for almost 40 percent of the patient, even you have the very initial good outcomes or for failed ablation. So that's why right now, especially based on the ECG findings, especially with the, we have a lot of the criteria, of course, not one of the ECG criteria to be 100 percent guaranteed that totally to be a LV submit origin, but if for those cases, we're supposed to be the LV submit, probably we will directly prepare the alcohol ingestion at the same time. So I think the benefit is that probably we could also get benefit, especially for the recurrent cases, that additional benefit, even if we get the initial successful ablation, but the difficulty is that it will be time-consuming, because probably even without additional alcohol ablation, that the patient still gets a procedure success. What do you think, on average, is the time added for ethanol ablation? Yeah, it depends on the interventionist. Usually we collaborate with the interventionist, and I think there is also one publication from China showing that it's the, there is a learning curve probably to be 15 to 20. Yeah. Great. Any questions? I have one question to the gentleman again. How did you think about the amiodarone in this issue you just mentioned, for the hypertrophic cardiomyopathy for the amiodarone or the catheter ablation? Is any comparison about it? Yes. So I think for patients with hypertrophic cardiomyopathy, a catheter ablation has clearly been demonstrated to be effective for both AFib and VT. The success rates are lower in patients with intramural substrates, and oftentimes, epicardial ablation is necessary, or some of these techniques, including ethanol, bipolar ablation, half-normal saline, now pulse field ablation. So certainly, and ultra-low cryo, other techniques to get deep in tissue. We generally will offer catheter ablation very early on, especially in young patients. From a risk-benefit standpoint, I think for having a 40-year-old with hypertrophic cardiomyopathy is going to do much worse on long-term amiodarone than undergo an ablation. It's not until they fail an ablation that we usually reach for amiodarone. Sotal, on the other hand, we will use very frequently. Okay. Thank you. I have one question for Dr. Zhou. It's funny that when we're in the CCU and we're treating patients with sick heart failure, you know, we always teach, never treat blood pressure. But then all of a sudden, we go to the EP lab, and then we're, the only data points we have are heart rate and blood pressure. So how often do you use the more important, you know, do you use prophylactic swan gans catheterization, mixed venous, in the EP lab? We actually, one of my colleagues, Dr. Neet Sandhu, had kind of put together a protocol where we would do that, you know, for every VT ablation case. The lift for that is a little higher, you know, because it's another thing that we have to introduce, another potential complication point. So we've kind of gotten away from doing that routinely. We are often monitoring blood gases, and there's some data for looking at kind of left atrial tracings, and just as another additive data point to kind of guide things. But you're right. Like, and honestly, too, the blood pressure is managed predominantly, if you don't like intervene, by anesthesiologists who are used to doing ortho procedures sometimes, you know, or OB-GYN procedures, and they aren't as well trained, you know, to kind of manage the sick heart hypotension. Yeah, I'm a big fan of putting in a, especially for the higher risk, I don't do it routinely, but for the higher risk patients, I put in a swan and just leave it in from the groin. Don't wedge it, but leave it in the PA, just so you can, because you'll often see, long before the patient collapses, you'll see gradual elevation in their PA diastolics, and that can be a good sign to either get out or change your therapy. Yeah, there's a couple other things I want to mention to kind of piggyback on Dr. Zou's discussion. One is the six-hour mark. Typically at most institutions, once you get to a certain point in time, your anesthesia coverage changes to the nighttime anesthesiologist, and I think that probably does play a role. We notice that if you do cases beyond 5, 6, 7 p.m., oftentimes you have a brand new team that comes in who may or may not be cardiac-related, but they're just the night team. So that's something to keep in mind. The other thing that we started doing recently over the last couple years, since the JAC paper was published by Rod Tung's group, was a lot of patients will have a paradoxical vagal sympatholytic response to VT, where the sinus rate actually goes down. So oftentimes, if you're going to do induction, if you pretreat them with atropine or glycopyrrolate, you can prevent that vasoplegic response that's related to basically a vagal response. So we found that to be helpful in some cases. I have another question for Dr. Winters. Because most of the time we mention about heart failure, especially for a deaf heart failure, but is it for a right heart failure, the EP procedure, the anesthesia, maybe another issue because it's more difficult. How about you think about this? That's absolutely true, especially in Colorado, we tend to have higher PA pressures. And that makes it even worse. And so I think the margin for error there is even smaller. But the same concepts apply. They can't do things that will kind of increase the work of either side. But the right side is usually neglected. It shouldn't be. I think the right side, too, is also, remember, with repetitive defibrillations, the right side is far more vulnerable to RV dysfunction than the left side. Both are vulnerable, but it's important to consider. Perfect. Yeah. Thanks very much for your attention and a great group of speakers. Thank you very much. Thank you.

materialism management

clinical outcome

ventricular arrhythmia

epicardial ablation

antiarrhythmic drugs

ventricular tachycardia

structural heart disease

hemodynamic stability

procedural techniques

cardiac conditions