Hi, I'm Eric Prostowski. Welcome to a new segment of EP on EP. It's a delight to have with me someone I've known for decades, Dr. Wee Nadamani, who was currently professor of medicine at Chulalongkorn University in Thailand. Wee, thanks for joining the show. Thank you for having me. It's a great honor. Well, you're so kind to say so. We're going to talk today about your pioneering work in ablation in Brugada. When we all started thinking about Brugada, the prevailing opinion was this was a phase two reentry. At some point you said, I don't think so. So why don't you give the audience at least some background before we get into the procedure of how you came to that? Okay. Well, after a decade of depolarization theory as a prevailing mechanism, there was a patient in Europe from Pedro Brugada Laboratory that had electrical storm and need a heart transplant because of that, because there was no other treatment. They sent the transplanted heart to Amsterdam Medical Center and the work of that group led by Ruben Cornell did the total heart mapping. As you know, they are well known on that. So they found no depolarization abnormality, instead they found depolarization. Fibrosis, I'm guessing? That's all fibrosis, yes. That was the first time that it was clearly documented. That's only one case, and then subsequently there was another case. But anyway, there started a controversy or a debate between depolarization and repolarization. Obviously the Amsterdam, Ruben, Jack DeBacker, and all that started depolarization theory. When I saw that, regardless of depolarization or repolarization, everybody agrees that the RVOT was a site. It's a site that's a subject, must be, regardless of theory. So I got lucky in a way that one time I was in Bangkok, there was a patient who had an electrical storm. Instead of sending him to a heart transplant, we just had to do something. We didn't have quinidine and the patient felt everything. So I took a patient into the lab. We have the emergency IRB approval and all that. We went using Salsa technique, and when I put a catheter into the RVOT, and lo and behold, we saw a fraction of the electrograms, and when we ablated, we normalized the Brugada ECG pattern, prevent the recurrence of VF, and we couldn't even do VF afterward. Can I stop you there? With fibrosis, I'm guessing, did you try to see if before doing all that you could actually induce an arrhythmia, or did you leave it alone and just ablate? No, actually, that patient only had spontaneous VF, but also we did VT induction, because at the time, to set up the protocol to get the IRB approval, we have to set up the criteria. One of the criteria is to normalize, if we can, or prevent inducibility. That patient, so we did a VT induction and we induced VF, basically. And after the ablation, the patient, we could not reinduce. So you did, I assume, you just ablated the entire area where you thought there was potentials? That patient, I couldn't say that I did the entire area, okay? I must be honest. Yeah. Because I was so excited, and then when I saw that, so I ablated. Because the extent of the ablation of that patient, it was not the same as I'm doing it now. As you're doing it now, exactly. Okay. It's unbelievable to see the Bugatta pattern disappear. Oh, God. It must have been a moment, right? And Eric, I'm a very slow writer. My former mentor always said, I'm a promising fellow, but never, just promise never do anything. But anyway, it was tempting to write a case report, but I was so afraid it was a fluke. So I waited until egg patient. And then you wrote it. And then wrote it. And then it was published in circulation that you know. Can I stop you for a second? Because if I go back in era, I remember when, now, I didn't start WPW surgery at all. Obviously, I came in later, but I trained at Duke with Will Sealy and John Gallagher. And I remember the first time as a trainee going in and watching him cut a pathway and a delta wave goes away. And it's a moment, right? Right. I mean, so you were the innovator though in this one. I mean, it must have been, I can imagine, so exciting because it really did two things at once. You cured the patient of their terrible arrhythmia, and at the same time, the substrate you ablated took away the Bugatta ECG pattern. Right. Though you don't, it's hard to do. All those theories of why you had Bugatta ECG pattern sort of melted away, right? Well, not really. The depolarization size still have a lot of doubt. And then there's, and in the speculation, Charlie said, well, we could see the fraction of the signal also. But anyway, so, but later on, we had an opportunity that came upon us because we could not, in some patient, we could not gain an access into the pericardium. Okay. And percutaneously. So we elected to take the patient to the lab because the patient have multiple VF episodes. Lab or surgery? Surgery. Surgery. I'm sorry. Okay. We have some patient who infected leads that we need to explain it. Okay. I took the patient to the OR, and the surgeon did a mini-toracotomy, and we did the mapping in the RV. Just like the WPW, the UV, we use a catheter and electrode, and then we just go, we create the grid over the CT of the heart, and we found fraction of the signal. We did a biopsy before we ablate. And there was fibrosis? And then the fibrosis. That's great. That's really great. The fibrosis is typical for the buccata, was the epicardial fibrosis and interstitial fibrosis. And that explain, as you know, when you see fraction of the signal, you know, the word, you know, it's a six-second impulse. And then at the same time, Professor Akihiko Nokami in Japan also found the same thing. Same thing? Found the same thing. And then they come by, and at that time, we also joined with the St. George University in London with Professor Raja Bae and his team. They did the study in the sudden death victim that have family, buccata family history. And they also found fibrosis, increased collagen. And also, when they did the immunohistochemistry to look at the connection 43, they found the problem. Found the problem. I want to take you back to, I don't know if you were in this era with signal averaging started. There were some early reports of positive signal averaging late potentials in buccata patients that was there. And people were like, is that just an error of the technique that, you know, but actually that was probably all. Absolutely. You got it. You hit it right in the nail. It was there. Yeah. But that is funny because I think I was one of the, you know, well, because I, the repolarization from the West population, it was very, very impressive. So when you see the signal averaging, we think, well, you know, may not be real, you know, things like that. That's exactly right. People question it. So wonderful start of this discussion. Let's take it to like now. So which patients do you decide to do an epicardial ablation on with buccata? How do you figure out who to take? The patient who has recurrent VF and has ICD discharges, that patient should be treated. For very simple reason, there is no other treatment because ICD doesn't prevent VF. Quinidine may prevent VF, but it's not available. Actually worldwide now, it's not available. Yeah, I find that amazing. We still fortunately have it, you know, in the United States. But even in the U.S., it's hard to get at times. Exactly. And not only that, I'll tell you something which you'll be amazed at because you and I did start to also grow up in a drug era that I sent a patient at the hospital to start quinidine and one of my younger EP partners called me and said, well, like, how do I do that? Even if it's available, it hasn't been used by most people. So let's take you procedurally then. What is your end point? When you're in there, do you use procainamide? Do you have to get rid of the buccata pattern? What do you use as an end point? Absolutely. The end point now is the fractionated, mapping all the area of fractionated electrograms. When we did first published in circulation of egg patient, I make one conclusion which had to be corrected later on. And that conclusion was that the abnormal substrate that exhibited fractionated electrogram was exclusively in the RVOT. But at the epicardium. But as it turned out, not true. Because later on when we used, in Thailand, we used aspirin. And we could see now the substrate is also extended to the RV body. And in some, about 29% also in the inferior wall. So that's where I think in U.S. we'd probably use procainamide for that reason. And then you'll ablate those areas also. Absolutely. And then the end point now is to eliminate all the area that show fractionated electrogram with after the sodium channel blockade. And has your experience been when you do that, the regatta pattern is gone? Right. That's fantastic. Yeah. What's the follow-up? How many people who you do that and you get it done will have no more arrhythmias? Well here, I just finished analyzing and writing it up right now. We have the... Oh, you want me not to ask? No, no. I can mention because I presented it as abstract. Oh, okay. But I thought so that the viewer could appreciate the result. We have 159 patients from the multi-sites from Europe, U.S. and also from Asia, mostly from Asia. And just in a nutshell, we found that patient in whom we can normalize the ECG pattern, that is only predictor of no recurrent VF. And is it like 100% prediction or close? In this data, almost 100%. That's unbelievable. We have one page, 98%, we have only one patient that had recurrent VF. That patient had also concomitant early depolarization syndrome. Oh, okay. So more than one thing. I have to tell the viewer also that, especially in Southeast Asia, regatta syndrome commonly have combined syndrome, about 20% to 30%. I got you. So if you have pure regatta syndrome without concomitant early lipo, if you ... Then you have a great follow-up. Yeah. We, pioneering work, so important to patient care. Thank you for your hard work and thanks for joining us today. Thank you so much.

ablation

Brugada syndrome

Salsa technique

electrical storm

ECG pattern