Good afternoon, we will continue with the session on anticoagulant management. He is a cardiologist and electrophysiologist at McGill University in Montreal, Canada. He will talk to us about anticoagulation during the implantation of devices. Go ahead, Dr. Vidal. Thank you very much for the opportunity to speak with you again. In this session, I will talk about the management of anticoagulation and how it can be used in patients who come to have implantation or replacement of heart devices. My conflicts of interest are here, and this particular topic is one that I have been studying for several years, and I am going to make a summary of the journey of my research in this field. We know that the use of these heart devices has increased over the years. With the aging population, more steps are used and with the indications of respirators, of synchro, etc., the rate of use of heart devices has increased. Also, with the advances in anticoagulation, many of these patients are anticoagulated. In the population of Marcapasos, it is the fourth of those patients who take anticoagulants, and in the group of patients who are candidates for a respirator, it is up to a third of the patients who are using anticoagulation. In the past, before the new oral anticoagulants, there was warfarin, and the clinical practice was always that, for any surgical procedure, warfarin was stopped and in patients at high risk of thromboembolism, a strategy of puenteconeparina was used. Here we see the guides of 2008, of the CHEST, which recommended that patients with moderate or high risk of thromboembolism, those groups of patients with mechanical babula or with a CHADS score of at least 3, that in those groups of patients recommended the use of a puenteconeparina. The problem is that we know that those types of patients are more at risk of having a pocket hematoma. And it is not only a matter of aesthetically looking bad or of pain, but it is something very serious because it is associated with a very important risk of infection. Also, paradoxically, when the hematoma arrives, the anticoagulation and increases the risk of cardiomyopathy, which we are trying to prevent. At that time, in Canada, we sat down with some friends, electrophysiologists, in a congress, and we started talking about what you do, how you manage those patients, and we sent a survey with various types of cases to see how the management of the patients was in Canada. And what we saw was that there was a very important variability in the management. Some, depending on the type of case, here are two different cases, some used puenteconeparina, some started to operate without stopping the warfarin, some stopped a little more than others, running perhaps a higher risk of cardiomyopathy. But that variability and that, in English we would say clinical equipoise, which means that there are quite a few differences of opinion that can be allowed, ethically and scientifically, to design a randomized study to compare the two options. And that was what we designed the BRUCE Control 1 study, the first one we did. It was a study designed to answer that question. An international multicentric study where we included specifically that group of patients that in the guides I presented in 2008 recommended puenteconeparina. The standard of care was puenteconeparina in patients with a risk greater than 5% per year of thromboembolism. We divided in two groups, the patient with the standard group was puenteconeparina, we stopped the warfarin 5 days before the procedure, we started eparina under molecular weight or intravenous before the procedure, it was done without eparina, without warfarin, after the procedure, at 24 hours we restarted eparina until the warfarin took effect and the INR went up in the therapeutic range of the patient. The experimental group was the group in which we decided to operate without stopping the warfarin, we had a target of an INR of less than 3 per patient in general and less than 3.5 in the mechanical valves. Patients with cropridogel the plan was to stop them 5 days before the procedure, if it was already more than a year since the stent and the aspirin was not stopped. The study was finished early in the second interim analysis, after having randomized almost 700 patients, all with a very good follow-up until the end of the study. The primary endpoint was a clinically significant hematoma that was reduced by 80% in the group that was operated without stopping warfarin. The definition of the primary endpoint was any of those three components of the primary endpoint, that is, a hematoma that caused an extension of the hospitalization for more than one day, a hematoma that required a complete anti-coagulation for more than one day, or a hematoma that had the need to re-operate, to intervene to evacuate the hematoma. The interesting thing is that also the three components of the primary endpoint were also reduced by 80% and all significantly. We analyzed all the subgroups of those patients and they all had benefits. Age, older or younger, sex, anti-inflammatory cones, all types of devices, whether they participated or not, whether the procedure was short or long, mechanical valve, in all subgroups it was better to operate without stopping warfarin. The summary of the BRUCE 1 study was that in those patients with a high risk of more than 5% of annual cardiomyopathy, we could reduce the risk of hematoma from 80% to 16% to 3.5%. We also saw that operating with an INR of more than 2% is safe and that it can be done. Therefore, since then, the recommendation is never to put a bridge with heparin after a procedure. Our fellows also published a meta-analysis of all the observational studies, including the BRUCE, which evaluated this issue and the results are quite clear that the bridge with heparin must be avoided. Another meta-analysis evaluated different strategies and here, in terms of the risk of hematoma, a bridge compared to not using a bridge increases the risk of hematoma. Stopping warfarin did not have much impact on the risk of hematoma and a continuous warfarin compared to a bridge with heparin decreased the risk of hematoma. But we have to remember the other part of the equation, that of ACV or deep venous thrombosis, that if a bridge is made with heparin, it decreases. If warfarin is continued, it decreases. If warfarin is continued, it is similar to a bridge with heparin. So you have more effectiveness in preventing hematoma, while maintaining the safety of preventing cardiomyopathy. In terms of cost-effectiveness, it is one of the rare studies where it is not only cost-effective, but also cheaper to avoid a bridge with heparin. So there is no doubt about what has to be done. We also publish that the rate of infection in patients with hematoma is 8 times higher than in patients without hematoma. Based on that, we recommend some guides based on the risk control of how to manage those patients according to the cardio-embolic risk, and also with some tips that you can, for example, take a few days before to try to have it in the normal range, but in the lower part of that range. These recommendations were adopted in the international guides, using the same algorithm. Then we got interested in the new oral anticoagulants. They are no longer so new, but we did the same, a Canadian survey in Brazil, which evaluated the management and we saw that in Canada there was also a variability of how those drugs were managed. Some of them operated non-stop, but in general they stopped according to the renal function. We did a sub-analysis of Rely in those patients who had a hematoma, looking at the rates in patients with Dibetran, we found that Puente with Heparin increased the risk of hematoma, but those who were treated with the new oral anticoagulant did not have many hematomas. Those recommendations according to the renal function and the type of medication, and we ended up doing the BRUCE Control 2. The BRUCE Control 2 was the study that we randomized without stopping the oral anticoagulant or stopping it a day before and a day after. The time without anticoagulation or without taking medication was a total of 72 hours between the last and the next, but in the continuous group they took the medication in the morning, they operated and continued taking it in the next dose. The group of patients had a score of almost 4. The results here you can see the interdose time of 72 hours in the interrupted group and 12 hours in the other group because they did not stop any dose. It was published here in the European Journal and this study was also finished early due to futility, because there was no difference between the two groups. 2% of hematoma in each group. Then we analyzed the two studies combined, the first and the second and here we analyzed in particular the risk factors of hematoma combining the two studies. What stands out is this line here of the association of anti-plaque with anticoagulants and patients who take anticoagulants have twice more risk of hematoma if they are taking anti-plaque with anticoagulants. This editorial summarizes the data risk of hematoma in blue and infection in red, doaxolito has low risk of hematoma, warfarin a little more, anticoagulants with anti-plaque the risk increases and puenteconephrine is the worst and must be avoided. But also the risk of infection is related to that. The RAPID did a post hoc analysis looking at the hematomas and they saw, although the definition of hematoma was well defined, they also saw the same pattern of association with anti-plaque. This question of anti-plaque is very important. We analyzed in the initial BRUCE the indications of anti-plaque combined with anticoagulation according to the current guides and we know that in the last years we have relaxed the intensity of double and triple post-therapy procedures and using the current guides we see that there are some patients in which anti-plaque is not necessary or it could potentially at least stop perioperative. To summarize and finish the BRUCE Control 1 study demonstrated that a strategy with the continuous use of borphaline reduced the risk of clinically significant hematoma by 80% compared to the BRUCE with heparin, which obviously should not be used anymore. The BRUCE II showed that there is no significant difference between the BRUCE and the BRUCE II. DOAC leaves the possibility and the option to the doctor to decide what to do according to the patient's thromboembolic risk and according to the urgency of the procedure. But one can proceed to do it without stopping if it is urgent or if the patient is at high risk. The point about the anti-plaque therapy is essential. There are patients who are with double or triple therapy, which perhaps is not essential. And although you do not have to change their medical management forever, at least a week before and after the procedure, the anti-plaque therapy can be interrupted to reduce the risk of hematoma by 50%. So, these are the points I wanted to communicate. I thank you very much and the collaborators in these studies. Thank you very much. Thank you very much, Dr. Eisenbahn. Now, the next speaker will be virtual. He is Dr. Carlos Morillos, from Canada. Carlos is from Bogotá. He is a reference in syncope and chagas throughout Latin America. Hello, Carlos. How are you? Mariana is speaking to you. Hello, Mariana. How are you? He is going to talk to us about the study… Spritely. I don't know how to say it. Spritely. Spritely. I need… I need you to allow me to share the screen, because otherwise I cannot show my slides. Can you hear me? Ready. Let's see if… Here it is. Well, thank you very much, first of all, Lars, for the invitation, and Somek. Unfortunately, I could not accompany you live for various reasons, but well. So, I have been given the task of talking about the Spritely study. The Spritely study was a study where we compared marks, steps against the implantable monitor in patients with syncope. This is a study that was conducted primarily in Canada. These are my conflicts of interest, including that I have been working in syncope since 1986, and I was a member of the executive committee and one of the main investigators of this study. Who are these patients? This is a 74-year-old patient who is in the emergency room because he has had a couple of syncope patients who do not have a major prodrome, they are from the beginning to the abrupt, they do not have a major family history or medical history, they do not have hypertension, hypertension, they do not take any drugs, they have a severe craniocephalic trauma, and an electrocardiogram is taken that shows what we see here, which is a complete left-brain blockage with a bifascicular blockage. This patient is then randomized in the Spritely study, which I will now show you the design, and receives a step mark. But what other things would one recommend? An electrocephalogram, a CT scan of the brain, Holter, an implantable monitor, a tilt, an electrophysiological study, or directly go to a step mark? It is still very controversial. This patient, because he had a craniocephalic trauma, a brain image is taken, and he has an intracerebral and subdural hematoma, which is significant. The patient receives his bicameral step mark, and three months later, there is a recurrence of the syncope. Of course, one thinks that the cable has moved, the interrogation is done, the cable is very good, it almost does not step mark, the x-ray is fine, a mesovascular test is done, which has a vasodepressive response, despite being stimulated. So now what do we do? We give him Midorin, Florinef, because this patient does not improve with the step mark. And when he comes to me for the consultation, I give him a clinical history, and I ask the wife, what happens to him when he faints? And she says that he has a workshop there in the garage, and when he is in the garage, he raises his gaze towards the ceiling, and when he is going to pick up a tool, when he faints. So we do an angiography here, for resonance, and we clearly show a subclavicle theft syndrome. So not everything that shines is gold. So it is still important to continue doing the clinical history as such, despite the fact that the patient had a blockage and fascicular, because that was not his primary cause. So what do we know about the management of these patients who have a syncope and a bifascicular blockage? Whether or not we should do a step mark, we must observe, or we must put a syncope implantable monitoring. Again, here is one with a right branch blockage, and a bifascicular blockage. In fact, with a prolonged PR, this patient benefits from a step mark or not. If we look at the recommendations of the European Cardiology Association, these patients with a syncope, who have had a previous heart attack, or other conditions that have healing, an electrophysiological study is indicated. This is class 1, but this is more to rule out ventricular tachycardia. But patients with a syncope, and bifascicular blockage, the electrophysiological study is recommended when the syncope remains unexplained, with an indication 2A. The reality is that in North America, in Canada, we use the electrophysiological study with these patients very rarely. And here is another recommendation that says that patients with an unexplained syncope, bifascicular blockage, a step mark is indicated if they have an interval HB greater than or equal to 70 milliseconds, or a third-degree blockage when incremental atrial stimulation is done, or with pharmacological stimulation. Again, this is a class 1 recommendation, but in North America we do that rather little. The group with Bob Sheldon and the Calgary group did a meta-analysis, looking at the value of the electrophysiological study, and it really is quite neutral in this population. What was the Spritely study, which means syncope pacing, or recording in the later years, that is, to stimulate or monitor in patients who are older. So we collected patients with bifascicular syncope at an age with a fraction of vision greater than 35%, and we randomized them one-by-one to an implantable monitor or a step mark. If there was no radicardic syncope or arrhythmic syncope, then they did other diagnostic questions. This study, then, obviously, what I wanted was to establish which of these two strategies should be first. Implantable monitor, which is primum non nocere, that is, first not to hurt, or the permanent step mark, which is primum succere, which is first to be successful. The inclusion criteria were more than one syncope episode in the previous year, a bifascicular blockade in the electrocardiogram of 12 derivations, being over 50 years, as the patient we described. The primary outcome, this was a pragmatic study, and this cost us a lot of work for the reviewers of various journals to understand it until it was finally published, because this was a combined outcome, as you can see there, of syncope, asymptomatic radicardia that led to an intervention, asymptomatic radicardia that led to an intervention, and this was more than anything else, systoles or intermittent blockades, and acute or chronic complications of the intervention and cardiovascular death. As you can see, there are several links in one. Almost 60 patients were randomized in both arms. This was a 75-year-old population with a standard deviation of 9, 20% women, and notice that they were patients who had not had repeated syncope, they were patients with an average of syncope in their life only of 12 episodes in the previous year, duration of the symptoms only one year, so this is a more abrupt presentation, one thinks that due to the clinical presentation and more abrupt, it is something of a cardiac origin, especially of the origin of conduction disorder. Left-brain blockade of 20%, a bifascicular blockade more or less in 40%. The primary desenase that I already showed you, which was that combination of syncope, etc., favored the step-by-step mark on the event monitor, and well, this was going to be logical because one says, well, this is what it does, is that the step-by-step mark prevents syncope, the monitor will not prevent anything. But surprise! It turns out that there was no difference in the recurrence of syncope with the step-by-step mark or with the implantable monitor. Of course, this misleads one, but wait a minute, these are patients with classic bifascicular blockade that would have a cardiac origin syncope, but it turns out that what happens is that these are harmful patients who have other things. So what was shown to me is that when there was actionable bradycardia, that is, it was bradycardia that had syncope, pre-syncope, etc., well, the step-by-step mark was obviously much higher than the event monitor, but there was no difference in cardiovascular mortality or complications in either arm. So in the primary desenase that is summarized here, you see the desenlaces in patients with primary desenlace was significant, but then when you see all the desenlaces, death, syncope, there were no significant differences. Symptomatic bradycardia that caused patients who had been first taken to an event monitor to need a step-by-step mark, well, this happened in more or less 12%, which was significant. Symptomatic bradycardia that did not cause crossover more or less also in 31%, and there were no major differences in complications, but obviously more in patients who received a step-by-step mark. And then, out of every 10 patients, 6 of these were going to need a step-by-step mark because it was bradycardia that was actionable, but they were all going to have syncope vasovagal, one died, one disappeared or ended up demented. So, what do we do with this in the end? Well, definitely, the step-by-step mark strategy seems to be better, but you have to know how to select these patients very well. So, to try to see, well, are some of these patients doing better than others? This is a study that has been published this year by one of my previous fellows from Argentina, the famous Dr. Adrian Baranchuk, and this is in the name of the post-stress group, which is the SPRITELY, looking at if the type of blockage only of the right-branch, left-branch, bifascicular, trifascicular, etc., had any difference or effect. And you see that there is no significant difference here. And here, blockage of the left-branch, in red, the step-by-step mark, the implantable monitor in blue, because the step-by-step mark is better, blockage of the right-branch, the same, bifascicular blockage, the same, the step-by-step mark wins more, bifascicular blockage, also. But remember that, obviously, it is to be expected that an implantable monitor will not have any effect when there is a need for a step-by-step mark. But here we see the probability of recurrence of syncope in patients who have blockage of the right-branch, blockage of the left-branch, in doses, and bifascicular or trifascicular blockage, and there is no difference. So, no matter the type of indication of heart disease, the step-by-step mark will work as such. Let's look at the European guides, where, even if the patient has bifascicular and syncope blockage, as I have explained, with a fraction of less than 35, there is no doubt, it must have a defibrillator or resynchronization, greater than 35%, here is where we still have difficulties. And the Spritely study, the only thing it tells us is that there will be a population that benefits from the step-by-step mark, but giving everyone a step-by-step mark empirically is not necessarily the best strategy. When doing an electrophysiological study, I reiterate, the meta-analyses we have done have not shown us that these patients benefit in a significant and important way. So, in short, what do we do with a patient who has bifascicular blockage and we want to try to investigate the cause? First, of course, the clinical history. Keep in mind that patients over 75 will have multiple causes of syncope. And it is likely that the step-by-step mark will help, but other causes must be ruled out, which are generally reflexes and can generally be handled by either reducing some drugs or simply handling reflex parts. So, this is what we have for now and the Spritely study has obviously led us to do other studies that we are currently doing. Well, thank you very much. Thank you. Thank you very much, Carlos. We will continue with the next speaker, Dr. Néstor López-Cabanilla, from Argentina. He works in the electrophysiology service of the Adventist Clinic of Buenos Aires and is a very strong reference of LARS. So, Néstor will speak to us. Néstor will speak to us. When do we have to... Yes, about total occlusions of veins and venoplasty for implantation of devices. Go ahead, doctor. Well, thank you very much for the invitation and thank you very much, Mariana, for the introduction. I will talk about how to put devices when there are occlusions and stenosis in the veins. So, in order to have a successful implant, we have to overcome problems that can arise mostly in the axillary vein, the subclavian vein, the cava vein, and for that we have to do a correct venogram, either by a peripheral vein of the arm, sometimes some jugular access, sometimes we have to do a femoral puncture and advance a long catheter to see the anatomy in a retrograde way. It is important to have tools, to know techniques, and to know how to implant the electrodes. So, it is very important that when we do a peripheral venogram, we often see a stenosis like this one, and we say, well, it's totally covered, but we shouldn't lose hope. Only in 20% of these venograms that show total occlusion, are they really occluded. When you advance a hydrophilic guide by axillary puncture, in 80% you manage to go through them, and more when you have a recanalization system, as I'm going to show you. So you shouldn't lose hope when you see a total occlusion. You have to have the right tools for the implant. And a very simple but very important tool that people don't use is to have a contrast injector, which is only two syringes linked with what we call a three-way key, an extender, and you always have to use this Y key. This is a daily use tool of the interventionist cardiologists that allows us to inject contrast and manipulate guides 0.14, 0.35, at the same time that a colleague injects us. We have to know the 0.14, 0.35 guides, the AMPLATS guide, which is fundamental, and this guide can't exist in the procedures. We have to know that there are hydrophilic catheters. This catheter K2 is extremely important, it's a short catheter with a hydrophilic tip that advances in the obstructions. The cobra catheter, which is very popular, is a totally hydrophilic catheter, but since it's not meshed, it doesn't have a body to be able to advance. Many times we need the laser system, which is a photograph of the system that is in the Incor Clinic, the Incor Hospital in San Pablo. And venoplasty is another technique, but it's mandatory. We have to know how to use it. There's no need for a hemodynamicist. It's something very simple, easy, and I hope to give you the most basic concepts. We have to know how to use the SNARES, the ties, and how to use these techniques to cross obstructions and stenosis. So, number one, venoplasty. Another very easy technique is abscising, how to go up from a 0.14 guide, which we were able to advance, to a 0.35 guide. We have to know that sometimes we can sacrifice an electrode that is already in the blood vessel, for example, advancing a guide, or use it in some way if that electrode is mobile in circulation and there's a stenosis that doesn't allow us to advance another electrode in parallel, we can use it, with techniques that I'm going to show you. And then there are some other tricks for complete occlusions. The basics of venoplasty are that there are two balloons, the complacent balloon and the non-complacent balloon. The complacent balloon is like a birthday party balloon that inflates, inflates, inflates, and has no limit. The balloon that we are going to use is the non-complacent balloon, which is like one of these beach balls that have a mold and a shape that allow us to squeeze force and be able to break a lesion. So, this is very important, use non-complacent balloons, always inflate at the breaking pressure, that is the maximum pressure that allows us to have the largest diameter and without breaking. The breaking pressure is the maximum pressure that we can inflate the balloon without breaking. The nominal pressure is the recommended pressure, but we always inflate at the breaking pressure. There are two balloons, the non-complacent balloon and the non-complacent balloon. The non-complacent balloon is very commonly used by interventionists for coronary stenosis. We are going to use the non-complacent balloon, where the whole body of the catheter advances on the non-complacent balloon. The non-complacent balloon is only a small portion. So, why is it necessary? It is necessary for many reasons. We are making more and more upgrades. There are patients who have a bicameral macrophage and we need to make an upgrade to a resynchronizer. It is very common that there is stenosis in the veins. So, in these cases, which are not primary implants, we see the need to be able to open the vessel in some way. And it's not just opening, sometimes a guide advances, but the intruder does not advance. So, it advances with great difficulty. And that will allow us to work in a comfortable way. The locations, we are going to see that many times they are in the distal region of the left subclavicle, many times an injury is added in the innominated vein, and sometimes it is only in the innominated vein. So, we have to try not to use incremental dilators with a larger diameter, a 7 French, a 9, a 12, because that gives us a real dilation of the vein, it gives us a false feeling that everything will be fine, and it will not be fine. We always have to do venoplasty. And in these distal obstructions, the small dilators do not reach, and we have to use, yes or yes, the venoplasty technique, always advancing in the form of digital venoplasty, then a little more proximal, and then half inside the pocket, and half outside the pocket, seeing us as if the ball is inflected in front of our eyes. So, in summary of venoplasty, always use non-complacent balls, on guide 035, my recommendation is always to use a ball of 6 mm in diameter, by 4 cm long, always try to use that ball, if you have to advance two electrodes, well, use a little more diameter, 9 mm is fine. Always advance in the union zone of the right auricle with the cava vein, the first venoplasty in that area, and then do successive venoplasties, getting closer and closer to the pocket. And always inflate the rupture pressure, which is the recommended pressure, for these cases. And always inflate until that waist disappears, and we see the vein completely open. Sometimes, only the venoplasty is not effective, then we need to resort to the focused force venoplasty, which itself is to advance in parallel to a ball, a guide, in this case, the common venoplasty did not work, here we advance a guide in parallel, and it gives that cutting balloon effect, it makes a cutting effect, when you inflate a ball against a guide. So, that's something important. Upsizing is very important, if somehow you advance a guide 014, you can advance over the guide to a hydrophilic catheter, remove the guide 014 and advance the guide 035. Let's see examples. Sometimes the ball does not advance, then you have to make an exchange. Then, the exchange advances over a guide of low diameter, then you advance a catheter, you remove the guide of low diameter, you advance a guide of greater diameter, like 035 amplas, which will give you support to advance the ball. Now let's see how we can take advantage when there is a free electrode in the venous access, that somehow we are not going to use, it moved, we can break it because we have to remove it and put another one, but how can we use that pre-existing electrode when you inject contrast and it does not advance, or when you advance a 035 guide in parallel with the electrode and it does not advance. We can use that pre-existing electrode to gain access without having to punch. This is a case that we did in Costa Rica, we advanced below the insulator of an electrode that we had to remove, we advanced a 014 guide, and then we advanced that electrode together with the guide to the circulation. Let's see how that advances, we see in that area how we remove the 014 guide, we disconnect it from the electrode, to put it in some way, and we remove the electrode, we already have a 014 guide in circulation, we advance a dilator or a hydrophilic catheter on the 014 guide to remove the 014 and advance a 035, so we already gain access. This is a patient with a resynchronizer, a left ventricular electrode displaced, but we can take advantage of it, advance the 014 guide beyond the tip of the electrode, remove the electrode, remember that the ventricular electrodes have a hole at the tip, and that's it, we already have the 014 guide, we advance a hydrophilic guide, we remove the 014, we advance 035, we do venoplasty and that's it, we are already in the light without having to punch. For example, sometimes there is an electrode that must be removed, and we can advance a guide in this electrode that must be removed, we can advance a 014 guide, and we can make an extraction below, and as we extract the electrode, the guide remains in the blood vessel. Then we can remove the electrode by femoral way and we keep the venous access. Sometimes, when the extraction is done, it must be done with a laser. This is a case of Dr. Roberto Costa, of the INCORP of San Pablo, where he made an extraction, but inside the laser extraction guide, he advanced a 035 guide to be able to do a venoplasty later and then place a stem. There are impossible cases to finish. In these impossible cases, when it is totally occluded, one tries to advance the guide and does not advance, and then what we do is use this recanalization system. It is very simple, it is two syringes with contrast, with an extension, joined to a dilator, 5 French, or ideally a catheter, each 2, hydrophilic. Then we do the puncture, we advance the guide, and on the guide, hydrophilic catheter, contrast, we advance the hydrophilic catheter, we inject contrast, we advance the hydrophilic guide, and we make successive advances of the catheter, guide, catheter, guide, always seeing with contrast, and seeing in different projections that we are always parallel to the pre-existing electrodes. This is an interesting case that I did with a medical colleague in Chile, a few months ago. It had all the occluded accesses, this is the right intercostal vein, the right subclavian was totally occluded, the left subclavian was also totally occluded. So, well, we went to inject through the previous jugular access, we used this hydrophilic catheter that I was telling you about, linked to the injection system, and you will see that the injection also through the previous jugular showed total occlusion of the cava vein. So it is an opportunity to re-channel. Re-channeling is a simple technique, as I told you earlier, it is only advancing a hydrophilic guide, advancing the hydrophilic catheter, injecting contrast, and advancing until we reach the cardiac cavities, always supervising in different projections. Once we manage to advance to the heart, we remove the hydrophilic guide and we advance a rigid amplas guide to be able to do venoplasty. So, in this case, the balloon is digitally advanced and I was doing successive venoplasties to dilate the entire upper cava vein. So, several venoplasties are boiling and we will go a little faster until we can dilate the entire upper cava vein. I got excited and said, well, let's see if we can re-channel the subclavian vein. So, what I did was with the re-channeling system, we did a more proximal function, total occlusion, more digitally, we were able to achieve the true light, I advanced a hydrophilic guide and I started doing venoplasties. The first venoplasty was of focused force, it was with the cutting balloon effect, because I was inflating the balloon against a guide in the vein. And then, you will see, the stenosis is very important and I did successive venoplasties until it was more proximal. So, finally, when it is totally occluded, there is a laser that does not go over the guide and allows us, in the case of having an obstruction that we see is very small, because of the re-channeling of the inominated vein and because of the previous re-channeling, we see that it is a small obstruction that does not go over the guide, we can advance a laser to get from where the laser is to this catheter that is in a re-channeled form. When the jump is small, we can use this laser, which is not the common laser for the extraction of electrodes. So, another last case is this case of total occlusion, the need to upgrade the re-channeler. So, it is very important to look if there is a patent Marshall vein. The Marshall vein is not the persistent upper left vein that we are looking for, but a small vein, which is the Marshall vein, that reaches the subclavian vein. So, when there is total occlusion, look for it. With a vein selector catheter, we can identify it, look for it, try to advance a guide that will take us to the coronary vein, and then, with a telescope system, we can implant the electrode in the coronary vein. To finish, always try to use contrast, make a correct veinogram to see the anatomy, to see what we are dealing with, and not just push and pray that we go to the right place. It is necessary to have the techniques, to know the techniques, to have the tools, to know what a veinoplasty is, to avoid an epicardial implant, or not to be able to do everything one has to do. There are tools, as I showed you at the end, for total occlusions, and remember that the veinoplasty is something simple, and that it has to be done by ourselves. Thank you. Thank you very much, Dr. Néstor López. A very quick notice, the people who were in the talk of Dr. Brugada, who participated in the Electrodes contest, the results will be in the Salón Girasoles, at 1.20 p.m., finishing the symposium. Well, let's go with our last participant of this symposium. It is Dr. Chang Dong, Director of the Department of Arrhythmias, Director of the Center for Auricular Fibrillation in Xiamen, at the University of Xiamen. Go ahead, doctor. Distinguished Chairman, Dr. Nestor, ladies and gentlemen, I'm Dr. Dongchang from the Xiamen Cardiovascular Hospital. It's my first time to come to the Latin continent and beautiful Mexico, so it might be harder to be here. Today I will share the opinions for our VT with structural heart disease, which we should choose. I think it's not an operative direction. If you choose ICD, you don't need the ablation. Of course, on the contrary side, it's the same. I want to ask which might be the first, which might be optimal. Let's share several of the case. For first case, the female patient had hypertension, and they have several syncope, and in a small hospital, perform the CAG, CAG show normal, and she also had syncope and the VT and CPR, so the TPNI inquiries, she was misdiagnosed non-STEMI, and prescribed many drugs for secondary prevention or CHD. Of course, it's wrong. So the patient still has recurrent syncope and the VT, so he come to our hospital. We can see from the ECG, it's very interesting. You can see from the chest with V1 is positive, QS comorphology, but in the V1 and the AVL, no RVV. All the QS morphology is negative. What do we think so? What's the origin? It might be very, very close to the epicardium. It means left direction depolarization lack. Why lack? Might be origin from the epicardium. So if no VT, the ECG show the different type of morphology or the PVC, and the PVC burden is not very higher, and the UCG echo shows the EF decreased with EF of 43%, and we deleted left ventricle, and we also perform the MRA, it show the same, similar result. We can see that in the interventric septum and the left free wall, there is fibrosis. So what's the diagnosis? So CHD, no, no non-STEMI. It should be diagnosed with sustained ventricular tachycardia, syncope, and cardiomyopathy, heart failure, and hypertension. So what's your choice? For this patient, ICD, good. For ablation, maybe good. What's your first choice? Maybe different doctor have different choice. Let's go. So I will say, my opinion is ICD is not a treatment targeting for the cause on induction. So for the patient have the recurrent syncope and VT, we should perform the VT ablation, then implant the ICD. So it's our opinion. So we first ablation the endocardium as the VLT, but the VT from the epicardium. So we perform the dry pericardial puncture and perform the substrate mapping where you can see in the left free, mid, and very inferior wall, we can see very low voltage area and the scars. So in these areas, we also see lava potential, and the QS duration is very longer. So we perform the lava ablation and substrate modification. And after ablation, we couldn't induce any VT. And of course, after ablation procedure, the next time we implant the device, why not in the same day? Because hypermine might increase the risk of hemorrhage. So the next day, we perform the ICD implantation. So there are three years, no VT, no shock. Maybe ICD is a backup. I think it's necessary, but I still think ablation is effective for this patient. Okay, let's go to case two. This patient also has VT, might be from left posterior septum. So the same question, ICD on ablation. Of course, ablation first, then ICD, because the patient has recurrent VT, and we also can activate mapping, and I saw that the VT origin from left posterior papillary muscle. We can see the papillary muscle potential during PVC. And after ablation, no PVC and VT, and good, and following up, two years, no VT and syncope. And the third case is a DCM patient. He had a non- ischemic cardiomyopathy and heart failure, and he also implanted the ICD. So different doctor had different choice. So the patient had recurrent VT and syncope, but the doctor don't perform any ablation, just implant the ICD and you drug. But the patient still have recurrent VT, so what's your choice? Drug or ablation? Of course, ablation. But it's a regret, the patient refused epicardial mapping and the puncture. So we just perform the endocardial mapping, and we found a very, very larger area or low voltage. We perform the substituted modification. Following up, four months, no VT, no papillary, no syncope. But of course, after four months, the patient still have VT and ICD shock. Why? Because the patient refused epicardial puncture. This patient is from non- ischemic cardiomyopathy. Let's go to the case four. It's a male. The patient has several diseases. Diabetes and stroke, and myocardial wall replacement, and the CABD. Two years ago, he come to my clinic for paroxysmal atrial fibrillation, and we perform ablation no recurrence. But recently, he still have the palpitations, and he showed no A-fib, but VT, and the heart rate is very fast, 117 pm. So it's very similar to the first case. So I think myology clinic's left lantern wall or the epicardium, might be epicardium. Because in either one, either AVL, no RV, all the QS complex is negative. But let's go to the next examination. From the echo, we can find left ventricle enlargement and the left appendix are neutral. So this is the answer. For the ischemic myocardial myopathy, the VT usually originate from endocardium, other than epicardium. Because the patient had an infection at the left ventricle apex aneurysm. So in the left apex, most myocardial infarct and the scar are cured. So no left directional depolarization. So in either one, either AVL, no positive view, no RV, just negative position. So the MRI showed a similar result, aneurysm. So the diagnosis for the basic disease is a coronary heart disease and the other myocardial infarction. At this basis, the patient had left apex aneurysm and sustained ventricle cancardia. So what's your choice? ICD? Might be right. Ablation? Might be right. Both. Which one might be first? We choose the ablation first, ICD second. So this is the GIBI show in the biggest congress in China, Great Wall Congress, we perform the GIBI show. So we perform the mapping and we find the left aneurysm, there is a large area of low voltage. And in the left anterior wall, there are also very big area of low voltage and scars. So we also find the lava, we can see lava potential, and the QRS duration is very longer. So after the substituent mapping and ablation, AVT could not be induced after ablation. Let's go to the case file. It's a patient from hypertrophic cardiomyopathy and 10 years ago, because the patient had myocarditis and AVB, he performed a pacemaker. And in three years, he had a recurrent disc pain and heart failure, so he needed an upgrade to the CRT. And after that, the patient had a recurrent VT. For this patient, what we should do is drug ablation. Of course, we need ablation. So this is very easy, because VT is just the origin from the left posterior septum. Let's go to case 6, coronary heart disease, recurrent palpitations, and VT, left EF, 38%. ACD arm ablation, ablation first. The oldest site is right of RVLT, only 15 milliseconds preceding the QRS complex. During ablation, PVC boarding decreased, but after ablation, PVC recurred. What we should do? Go to the left. Go to the left, but the oldest site is only 12 milliseconds preceding QRS. When we're mapping the AMC and the GCV, we perform an ablation, but still, the PVC could decrease, but we still can see the PVC recurred. So we just transplant the atrial septum and go to the left ventricle, and the performance occur, makes the tip cancer very contact to the left ventricle summit. After the anatomic ablation, the PVC disappeared, and no VT. Go to case 7, it's another patient with old myocardial infarction, and the recurrent VT. So this is the VT. So for this patient's coronary CT and the ECG, and we perform the every examination. What's your treatment? I see the ablation. We perform the ablation first. So we can see in the inferior or left wall is a large area of the vortices. It's consistent with the old myocardial infarction history. So the cancer, the QRS morphology, or VT, changed. Sometimes induced cancers might be touched in the caglium. We can induce a different morphology of QRS and the VT. So what we should do, we perform a substitution modification. And after eliminating all the lava potential, and all the low vortices and scar ablation, the patient couldn't induce any VT. And following up, the patient refused the ICD, but the patient is good. No VT recurrence, no syncope. The patient accepted several hotel examinations every year. It's good. Go to case 8. The patient also has old myocardial infarction, and still has VT. So the same questions. So we perform the left ventricle substrate mapping, and eliminate lava, and we also induce the VT. And during VT, we just perform the activation mapping, we find the ECS mass. We also perform the in-treatment, in-treatment to show the ECS. It's crucial, the ECS mass. So we perform the ablation. You can see the VT terminate, and the converter into synesthetism. So then, just targeting the low vortices area and the scars, we also perform substratum modification. So following up, one year, the patient had no palpitation, no VT, and the patient also implanted ICD, but no ICD shock. So let's go to review the VT with structural heart disease, and might be a patient that performed ischemic or non-ischemic cardiomyopathy, and cardiac ion channel pathy. What we should do? Most of the VT, just the mechanism is re-entry. And compared with LVC and the ischemic cardiomyopathy, DCM VT, the recurrence might be higher. Why? Because scar, sometimes a scar just in the mid-wall, so the endocardial ablation and epicardial ablation couldn't eliminate the scar, couldn't target the scar. So traditional guideline and the expert can say ICD is the first line consideration. Ablation only performed during the AAD failure and after the ICD implantation. But ICD have several limitations, it couldn't prevent VT and not the treatment for cause and induction. ICD shock, which result pain and anxiety, which increase hospitability and VT stop, and sometimes increase the mortality. In clinical study, VTEC show the patient's performance ablation could reduce the VT recurrence and the ICD shocks. So how to do that? The activation, in treatment, substitute modification are all my choice. And we also targeting the LAVA mapping and ablation. If we eliminate the LAVA, the long-term outcome might be good. Sometimes for the non-ischemic cardiomyopathy, we need EPI and endocardial ablation. What's the end point? Now VT induction might be better. So if no VT recur, both in the different left EF and the ischemic and non-ischemic, and the only H1 lead and 2 lead and the 3 grid, 4 grid, both patients, all the patients without VT induction has a better outcome during long-term following up. According to the guidelines, according to the past guidelines, ICD is the first choice. Just during ICD recurrence shock and VT recurrence, we perform the ablation. But with the many clinical outcomes, we should change. This is a very famous study. And post-ICD, just we first perform the ablation, then implant the ICD, we can see ablation growth could reduce the component end point, including VT recurrence, cardiovascular hospitalization, and death. So that's a very good study. And according to new guidelines, the case ablation level improved. And for the coronary heart disease, a case ablation might be the alternative treatment to ICD. So go to the question time. For the VT with a structural heart disease, which way should we do ICD ablation? Maybe we need both. But if the patient have recounted VT, we should choose cancer ablation might be the first. Go to summary. VT with ICD is still a challenge, and the structural heart disease and VT complexity and the progressing increase the risk of the VT recurrence. And the transmuralism might be hardly achieved. So ICD is still necessary, in my opinion. But ICD not treatment, of course, and induction and limitation is obvious. So with the evidence or clinical studies, we should perform cancer ablation as a first line during the recount VT recurrence before the ICD implantation. So what is the recount? More than twice. Okay, this is my lecture, and welcome to China, welcome to Xiamen. Thank you, thank you so much. Thank you.

ventricular tachycardia

structural heart disease

management

implantable cardioverter defibrillators

ICDs

catheter ablation

recurrent VT

arrhythmia induction

abnormal tissue

hospitalization