Welcome, everyone, to a session that is specifically dedicated to learning from mistakes that we might have encountered, complications that we've encountered during ablation procedures. We've got a wonderful and very experienced panel of experts to provide their insights about cases and complications that have helped to make them as great as they are. So Creating Diamonds from Dust, How Experts Manage Ablation Complications, I'd like to introduce the first speaker, which is Bill Miles from University of Florida. He's going to talk about how he managed and learned from his worst complication during SVT ablation. Well, I have an apology in a way because this isn't my worst complication, but this was a complication that I thought would be more interesting to present. The rest of my complications have been so routine and mundane that I thought this was a little bit better. So this is a 65-year-old woman with recurrent paroxysmal atrial fibrillation. She was referred for percutaneous closure of an ASD and evaluation in a congenital heart clinic, subsequently referred to EP for AFib ablation before ASD closure. Pulmonary vein isolation with radiofrequency ablation of complex fractional electrograms was performed. This was performed about 18 years ago, so the techniques were a little bit different. Cavotricuspid isthmus ablation. Patient did very well during the procedure, no hemodynamic changes. Just to show you the ancient nature of the procedure, that's a barium esophagram showing us where the esophagus is, a double transeptal with a lasso catheter and a radiofrequency catheter and other diagnostic catheters. And it's before the routine use of either ice or TEE during ablation. I keep going. So post-procedure, we got a routine echocardiogram, nothing in particular wrong. And the parasternal showed this abnormality in the echocardiogram. And the short axis shows the same abnormality. And the four-chamber view shows the same abnormality, a large abnormality in the left atrium. And this was interpreted as a large hypoechoic mass in the posterior left atrium compressing the left atrial wall. The mass is most likely a hematoma that's intramural within the coronary sinus or in the pericardial space posterior to the left atrium. Although the left atrium appears compressed, flow around the mass and across the mitral valve appears unobstructed. And there was no pericardial effusion. So we did a transesophageal echo. And this is what we saw. In the left atrium, there was this membrane going across here with echoes within that membrane and a very narrow space going toward the mitral valve. Couple of different views. Here's a view right here, mitral valve, big mass in the left atrium that we thought was an intramural hematoma. Here's a Doppler showing turbulent flow but no severe obstruction. Another view just showing another view of that mass. Here's the mitral valve over here. And one last view since they're all sort of ugly gorgeous. Big mass in the left atrium, mitral valve. All right. So the report was a secundum AST was seen. We knew that from before. A large mass, 4 by 7 centimeters, probable hematoma is seen posterior to the left atrium. Echolucencies are seen within the hematoma but no flow is identified within the hematoma. The left atrial wall is compressed. Flow around the mass and across the mitral valve is turbulent but not obstructed. Flow is demonstrated in the left upper and right upper and lower pulmonary veins. No pericardial effusion identified. So we got an MRI just to get a better look at it. And here's the left atrial mass in the MRI. Another view right here. Mitral valve, left ventricle down here, excuse me. Another view here. Again there's flow into the left ventricle from the left atrium. The left inferior pulmonary vein was stenosed but not totally occluded. The right inferior pulmonary vein was narrowed but not stenosed. The right superior vein and not shown here, the left superior veins were both wide open. So this was read as a hematoma within the posterior wall of the left atrium measured 7 by 4 by 8 centimeters in cross-sectional diameter. Stenosis of the left and right inferior veins secondary to the hematoma formation, worst on the left where the left inferior was narrowed to 3 millimeters and a large ASD. Because hematoma was intramural, not intraluminal. So we admitted the patient to the CCU, a PA catheter was placed for close monitoring. Pressures were normal. We reversed anticoagulation. The CT surgeons actually didn't want to touch her because they were afraid that the atrium would be very friable and the surgery would be a mess to do. And we treated her with frequent serial echocardiograms. She was managed conservatively with ICU observation but without any intervention. Echo at discharge showed that the material within the hematoma was organizing and there was a very small pericardial effusion. And three months later at the time of the ASD closure, the mass is gone. Some of the views show a little bit of something that might be a little bit of the posterior wall that was involved in the hematoma. So we look back at the literature and this was a report of an unusual complication from a catheter ablation. It looked very much like what I just showed you. This patient was hemodynamically unstable, was operated on, and did well. Here's another example of a patient that had a pericardial effusion. When the effusion was drained, that intramural hematoma was there, but it went away spontaneously over time without surgery. And here's the MRI from that particular case, similar to what we saw. Another report of a left atrial wall hematoma after RF ablation for atrial fib. Again, it looks very much like what I just showed you for our case. This one was also treated conservatively. And lastly, I'm going to show you there are a couple of these in the literature of atrial wall hematomas from procedures for total coronary obstructions. So trying to get through a coronary obstruction, they dissected into the left atrial wall. And again, it looks a lot like what I just showed you. And here's an MRI of that hematoma from the CTO procedure. So lessons learned. Well, one lesson I didn't put here is that you should be gentle in the left atrium. I'm not sure exactly what we dissected in this particular case. Atrial intramural hematoma is a rare complication of left atrial instrumentation. It represents a dissection of the atrial wall without necessarily perforation into the pericardial space. But there's a potential of mitral valve or pulmonary vein obstruction or rupture into the pericardial space. So the patients have to be monitored very carefully if this is discovered. However, if it's stable and asymptomatic like it was in this patient, the patient could be managed conservatively and the hematoma will gradually resorb. So thank you very much. Thank you very much for that presentation. I was neglect in not introducing myself and my co-chair. So Harris Hecani from Australia and Wendy Zou from Colorado. Harris, do you want to ask up the next speaker? Sure. Yeah, we'll leave questions for the discussion at the end, but keep them coming in on the app and we'll get to them all hopefully during the discussion. So it gives me great pleasure to introduce our next speaker, Professor Boris Schmidt from the CCB in Frankfurt, and he's going to present his worst complication during pulse field ablation. Thank you so much. Thank you very much for the kind introduction, ladies and gentlemen, and let me just start the presentation here. Today I'm going to present my worst complication that I experienced with pulse field ablation, and these are my disclosures. So what are we going to talk about? I'm reporting a case of a 63-year-old female patient that came to us for symptomatic paroxysmal atrial fibrillation ablation. Other than that, she had minor comorbidities such as heart failure with preserved left ventricular ejection fraction in a New York Heart Association functional class of one to two very minor symptoms. Her primary artery disease was recently ruled out invasively. She was on medication for arterial hypertension that was subsequently well-controlled, and she suffered from a chronic pain syndrome. The patient was a roll-in case in the omni-IRE study. Before the procedure, we took a baseline ECG which showed normal sinus rhythm at a normal heart rate, normal intervals, and no repolarization abnormalities, and as per our center standard, she received a transesophageal echocardiogram the day of the procedure to rule out intracardic thrombus, which was positive in this regard, so no thrombus present, normal emptying velocity of the left atrial appendage. There were no plagues in the aorta, and we did not have any evidence of ASD or PFO using a bubble test. So she subsequently underwent ablation using this large footprint PFA catheter applying bipolar pulse field energy, and the catheter is integrated into a 3D mapping system and is also equipped with a contact force sensor. Our procedure, as per standard, was performed in deep sedation using propofol, fentanyl, and midazolam, and the procedure itself was completely uneventful. We applied 33 applications to achieve circumferential, wide area circumferential pulmonary vein isolation on the right side, another 30 applications for the left side of pulmonary veins. Total procedure time was 105 minutes, including a 20-minute waiting period after the last energy application, and floor time was 9.5 minutes. During the procedure, we observed a rate-dependent left bundle branch block, but that went away with lower heart rates. During the procedure, the ACT was always above 300 seconds on the 327, excuse me, to be exact, after applying 12,000 units of unfractionated heparin. Patient, after the procedure was awake, she didn't have any signs of neurological deficits and after being completely awake, she was transferred to the telemetry ward. This is the picture of the 3D mapping and the energy applications, the ablation applications during the procedure complete 3D map with the circumferential wide area ablation. So after returning to the ward, half an hour later, you see a normal telemetry strip, normal sinus rhythm, the clock is given here, 5 o'clock in the afternoon or 5.50, 5 hours later, 7.40, we saw little elevated heart rate, patient was not complaining of anything, and the left bundle branch block that we also observed. During the procedure, another 1.5 hours later, once again, normal sinus rhythm, normal left bundle branch block with lower heart rate, 5.5 hours after the procedure, again, left bundle branch block, again, with higher heart rates, and then at 7 hours, she presented with, I would call it a shark fin ECG and bradycardia and very rapidly deteriorated and went into VF. The nurse on the ward alerted or did a CPR alert and the physicians from the ICU are usually coming to the ward and they started immediately resuscitation at midnight and pursued that for more than 30 minutes but could not reestablish any spontaneous circulation, so the patient was declared dead at 1.20 a.m. The reason for that, well, we can certainly discuss it. We speculated in many different directions and, of course, in these unclear circumstances, we obtained an orthopsy and the orthopsy showed a large inferior wall myocardial infarction. The patient had a dominant right coronary artery but there were no plagues and no intravascular thrombus was seen during orthopsy. She had no coronary artery disease whatsoever, also not on the left side. There was no signs of atrial esophageal fistula, no cardiac tamponade, no vascular lacerations, no evidence of stroke, and so the ultimate speculation that we had is that we have to deal here with a generalized coronary spasm after pulse field ablation, though we cannot prove it. I have to say that this is a phenomenon that is not, let's say, device-specific. It's rather energy-specific, obviously. It's a very rare complication that we see with this and other PFA technologies. You might have seen the late-breaking presentation of the Omni-IRE study with the regular cohort and it appeared to be a very safe technology. I want to highlight this here. In the other 136 patients, no serious complications were observed. We know that coronary artery spasm may occur with other PFA technologies, too. It's reported in the MANIFEST-70 case study with 0.14% and there were, of course, if you look into the literature, there are also other cases with PFA technology where coronary spasm was observed. There seems to be a distance-related effect. So if the coronary artery is within the electrical field, you can reliably induce coronary spasm and you can counteract this with nitroglycerin applications. But there are also cases such as this one that comes from our center where ablation with the pentaspline catheter at the pulmonary veins caused coronary spasm at the right coronary artery, resulting in ST elevations and complete heart block. Again, after intracoronary nitroglycerin application, it went away. And there are also other publications from Melanie Gunavadena right here with the same device and also another case from a UK group reporting a similar, let's say, event 45 minutes after pulse field ablation with the pentaspline catheter in a single patient. Coronary spasm may also occur with thermal ablation, though it seems to be quite rare, 0.19% during various occasions during an ablation or after an ablation procedures and the mechanisms are still quite unclear. So I would like to conclude that coronary spasm may occur with any PFA system at variable time points. There are proximity-related effects, which is most often, but there are also generalized spasm that seem to be unrelated to the electrical field directly. The time course seems to be quite variable. Measures for proximity-unrelated spasms remain to be determined. It's not well explained. Prevention measures for the proximity-related spasms include IV nitrates. For the generalized, we don't know. And the question in general is, with PFA ablation, is same-day discharge really an advisable strategy? And I hope to discuss this with you after the presentations. Thank you very much. Thank you. Thank you very much. I'd like to call Dr. Roderick Tung up to the stage from University of Arizona, who will be talking about what he learned from a complication from VT ablation. Well, these are heartbreaking, to be honest, when you listen to these, and I even heard there were gasps when people hear that we lost someone from an elective procedure. And I think there is a lot of courage to do this session. It's a great one because, you know, as Shiv always said, learn how to make new mistakes. We can't make the same ones over, and if there's anything that we can do, it's to learn from all of our collective mistakes. So I think this is a great session, but very difficult for me to share this one with you. So this is a 52-year-old, very active, very healthy woman with paroxysmal AFib, and she also had frequent PVCs detected on an outpatient holter. She was a very important member of our community and entrusted all the care with me. Symptomatic AFib episodes and really did not want to be on any antirhythmics. And the resting heart was 30 to 50 because she was so in shape, and that's why we didn't really think about beta blockers, calcium channel blockers, et cetera. We offered flecainide and had symptoms due to PVCs as well that she would feel as compensatory pause, et cetera. Undergoes successful PVI, and in that setting, we decide to also do the PVC. How many people here do multiple mechanisms in one procedure? So many. And actually, Shiv always taught me for nine years, don't do that. Like, just do what you're supposed to do, and don't try to do too much. This was the ablation that we did. We tried below the left coronary cusp for this LV Summit PVC. We had this far-field early ablation distal. So there's this far-field early that's about minus 20. You can see that there was frequency of the PVCs. This was performed after PVI, and here you've got a bigeminal, trigeminal pattern. Ablation comes on, and it's gone. Everyone feels pretty great. This was ablation number three because we had previously gone with two lesions below the left coronary cusp, and that was eliminated above the cusp. There were no temperature rises over 35. It was irrigated. The first two were below, as we talked about with transient suppression. Four total applications, 30 watts titrating up to 50 due to late suppression below the LCC. So it was late suppression. We went from 30 to 40. The second application was 40 up to 50, came back, and then we went above the LCC, and that's the lesion that you saw. It was gone in one second when we delivered it from above, and everything was great. Patient was discharged with routine anticoagulation. Everyone's happy. PVI was pretty much completely unremarkable. So three weeks after the PVI plus PVC ablation, the patient presents with tamponade. Three weeks later, and there's a large hemorrhagic effusion that we drain, which is very strange. I remember thinking, what is, this doesn't make any sense. I haven't seen this before. We put the drain in for three days, and then we empirically started some steroids for maybe like pericarditis or hemorrhagic Dressler's was the thought, that this is maybe a bad sympathetic or transitive effusion that bled on anticoagulation. And then we did imaging, and we were reassured that everything seemed normal, there weren't any mechanical complications that could cause this. And you would hope the story ends there beautifully. And patient goes home, a lot of reassurance with the husband as well. And then two weeks after that, which is five weeks now, status post PVI plus PVC, patient represents with a second tamponade. And large hemorrhagic effusion drained again, but almost lost consciousness, hypotensive in the ER. He comes in, and then we're like, I can't believe there's another effusion again. We decided to drain that, and really couldn't understand why there were these recurrent effusions. And I remember actually calling around, I think I called Luigi DiBiase, Andrea Natano, and say, have you ever seen like recurrent bloody effusions after this? And called many people, and we continued to try to reassure the family, but I didn't really know what the diagnosis is. I said, this might just be a really bad case of hemorrhagic Dressler syndrome. And couldn't find any other reasons as to doing so. So the patient goes home and is fine, and then ends up going to get a second opinion from Northwestern, our friends at Northwestern, that was at University of Chicago. And they decide to do an MRI, and we'd previously done CT scans. And the red arrow points to a large area that fills with contrast, and that is a large pseudo aneurysm of the left ventricle, of the basal LV. And it was so large that when we reviewed it, we re-reviewed our CT scans, our group actually said, we actually thought that was like left atrial appendage, and we missed it. So when you think about medical errors, they happen on multiple, multiple, multiple levels. There's so many decisions that could have been made. And so it was missed. And then the thought was, well, do we coil this? Do we do something that's innovative? But this is a large neck. It's not something that would really coil. You're already way out in deep water. And I think once you're in deep water, there's always that incentive to try to do something innovative. But sometimes you just want to do what you know is definitively fixed. This was the 3D reconstruction of this. And the red arrow here, so this points to the PA, then you get the appendage above. So you've got the pseudoaneurysm, this entire one that's below the left atrial appendage, but could be confused as the left atrial appendage, just this large structure. And here you can see it here sticking out with the appendage above. So Brad Knight calls me and said, you know, we've got your patient. And I was like, what did you find? And they go, oh, there's a massively large pseudoaneurysm. And you don't really know what to do there, because you've caused it. There is maybe we shouldn't even have ablated the darn PVC in the first place. Then we went up to 50 watts. So I went back and checked all the biophysical parameters. Was there a steam pop? There was nothing there. But you're just thinking, this should have just been a PVI. This should have just been a PVI. This is a healthy person. Why would we go after that? But she was symptomatic. And then Brad's like, do you think we could even write this up? You know, would you be fine with that? And I said, I think we should. I think we should, because there's so many areas I travel around the world, and I see 50 watts being delivered willy-nilly around the LV Summit all the time. And I don't think anyone's not guilty of that here. And I do mention this a lot of times in symposia to say, something terrible can happen. Something terrible can happen. And we wrote it up. We wrote it up. We did reports and heart rhythm case reports. And they asked me if I wanted to be a co-author. And I said, go ahead and put me on it, because I'm part of this. And you know, the patient and the family have never spoken to me again. And this is the nature of what we do. We always love to celebrate all of our successes. And she went to surgery and got a surgical repair, a Gore-Tex patch, everything. And things went really well for her overall, but she had a sternotomy that she never planned on to recurrent hemorrhagic pericardial fusions that Dr. Tong reassured them was Dressler's and everything was fine. So you know, there's so much loss in trust whenever you have to be the person that goes to talk to the patients and tells them what you think is going on. Then you have to think, well, how come we missed it on imaging? And you know, you don't want to throw your team under the bus. It's a team miss that you do. So I get really nervous about double indications. You know, the whole mommy makeover to make light of it, to try to do too much in one, I think is something that I get nervous about. And that's probably because of this case. This field can break you. And I remember calling Ken Ellenbogen, John Miller, because I actually thought that I was going to quit EP. I thought I was going to leave invasive and just be a non-invasive electrophysiologist because it was that heartbreaking for me. And it's obviously traumatic when I even think about it. And obviously, it got brought to legal attention as well, which is the first time I've ever been exposed to that. So you always just think, well, this is just a PVI. This is just a PVC. Just add it on. And we all have this workflow now where it's like, well, it's the fifth one. It's Friday. Let's just get through it. But this one case can break you and make you question your whole career. And mentors are really important. Because John Miller told me, he goes, Rod, if you quit, think about all the other people that won't be helped if you just quit right now. He goes, we've all been there. And it really is helpful to talk to people that have been there as well and been in really dark, dark places. And you're always one lesion away from being a hero or a complete zero. That one extra lesion that we call bonus, I actually laugh about it now. That bonus lesion, it may not be a bonus. It may actually destroy your career and someone's life. And own your complications fully. I'm grateful for the opportunity of this. You should never make light of these and just get used to them and be numb. I think a lot of times you do see people go, yeah, this just happens. It's so rare. But I think, you know, there's the right amount of emotion that you should have with these. That you really have to beat yourself up about these. But you got to keep going as well. And I'm living proof that I did. But I almost quit EP because of this case. And as Shiv says, learn how to make new mistakes. So thanks for the opportunity to share. Thanks so much, Rod. But just to take umbrage with one thing is the prerogative of the chair. Boris's case was just a PVI as well. So we just never. And so was Bill's. We're just never. We're just all blessed when a case goes well. Anyway, next up, Professor Kiyoko Tsujima from Tokyo gives me great honor to introduce her to speak about her worst complication during a PBC election as well. Thank you. Thank you very much. It's a very, I think, a heartbreaking session, but I agree with you. I think we have to share the complication and try not to repeat again. So hearing Roderick's story, one of my colleagues was kind enough to share this case. But this is one of the reasons he decided to leave the university hospital. So I'd like to share the case with you. So a 69-year-old male presented with palpitation. Previously, he underwent PV isolation, but now he's left with a PVC. And Holter monitoring showed a PVC burden of about 25%. So it looks like he has two types of PBC. One is probably positive concordance in the precordial lead, which is dominant. And the other one is a little bit high in 2,3-AVF and left bundleoid morphology. So we decided to place two French catheter into the anterior interventricular vein. So this is his pre-procedural imaging chest X-ray. And we usually have the CT scan because we want to merge with a 3D mapping system. What do you think? I thought it's a little bit, he has a ateloma plaque a little bit on the root, but nothing significant, a little bit of aortic elongation. So we placed a two French catheter into the AIV and a luminal catheter into the great cardiac vein. And what we found was for this PVC, the PVC1, which is a dominant one, a little bit difficult to see, but there is a CS78, which is located in this area with a tiny potential that precedes a QRS by 58 milliseconds. But we can't ablate in the great cardiac vein because it's so small. So we decided to map RV and probably the CS and then trying to get closer to this potential. So this is a time course during the procedure, 1250 we got access, femoral artery, femoral vein, and around 110 we started to do a transepto and LAV mapping. And the patient complained the back pain during the procedure. He's known to have some like a disc hernia, so we wanted to kind of keep him like comfortable, so we gave him a little bit of sedation. But he woke up again right after we did a retrograde approach and gave him a sedation a little bit. And he started to having a lot of atrial fibrillation despite a previous history of a PVI. So we started to do, again, it's similar to Roth's story. We did a retouch with a PV isolation, posterior wall ablation. And then we ablated for this PVC, RVOT, and CS, and it kind of, PVC is getting quiet, but so we decided to do the LV ablation and the PVC disappeared. But after that, his blood pressure dropped. So this is sinus rhythm without PVC, but right before the final ablation, his pressure dropped like very abruptly. So the echo showed a significant amount of pericardial fusion, cardiac tamponade, and pericardial synthesis did not stabilize the patient. And so we did have to put him to PCPS, and he was transferred to the emergent operation. But unfortunately, he did not survive. So this is what we have. Autopsy showed this is a brachiocephalic trunk, left common cardiac artery, a left subclavian artery. And you can see a little bit of a ateloma here, and there is a little crack. I wouldn't say little, but pathologists thought it could be caused by the housing prepared like a mechanical, but I think it's pretty sure our catheter have caused it. So it looks like the same vision here. So ateloma, probably when he struggled to pass the ablation catheter, tried to make a loop at the aortic route. I think that hit this ateloma and unfortunately, penetrated the aortic wall and caused a pericardial fusion tamponade. So I think possible causes for injury Avolta has, one is advancing ablation catheter to a descending aorta can result in trauma to the intima or dislodgement of aortic calcification. And also there is often insufficient space in the aorta to cause ablation catheter until the tip of the catheter has entered the aortic route, which we usually do. But calling the catheter tip within the route has a potential to cause traumatic damage to the coronary vessels and to the aorta. And finally, manipulating the ablation catheter to cross the aortic valve can cause traumatic disruption of the intima in the aortic route, resulting in antigrade aortic dissection. So there has been a case series, this is nicely depicted. So this is the area where they had iatrogenic arterial dissection, a little bit difficult to see, but like four cases here involves the ascending aorta and the four cases here involves the distal femoral artery. But overall, this is coming from 10 centers and the incidence is about 0.4 to 1%. So I know it's a little bit difficult to see, but I think majority of the patients did have no symptom, but a hypotension and pain. And like some patient is PVC, PVC seems to be a pretty dominant, and VT and SVT. And one patient died, not a good surgical candidate, and she passed away. So for final thoughts, I think it's very important the risk of injury to the aorta can be reduced by gentle manipulation of the ablation catheter into a pigtail shape, closer to the femoral access site, ideally using the contralateral common iliac artery, allowing the catheter to traverse the entire aorta and engage the aortic valve in a protected conformation. Thank you very much for your attention. Thanks very much to all the speakers, both for outstanding presentations, but also for owning the humility that Rod alluded to, to talk about these cases and for us all to learn from them. Because we all have stories like this, and if we don't have them now because of duration of experience, at some point we will. And so it's important to kind of discuss them. Does anyone have any questions? Anyone who has questions in the audience can feel free to come up to the microphone, or you can use the app and enter them online as well. I wanted to... Yeah, sure. No, you go ahead. There was a question, I guess, for Rod, from the audience already, so about how you know that it wasn't just a localized... Oh, sorry, that was Bill. How do you know... Well, there's several cases. So how do you know it wasn't a localized pericardial hematoma? Unless a patient goes to surgery, it's hard to say what it is. Yeah, it could have... Is this microphone working? It could have been a walled-off connection to the pericardial space, similar to a loculated But it was just so distinct, and on the CT scan, it didn't look like there was any involvement of the pericardium itself, that I think it was basically an undermining of the endocardium of the atrium, which allowed blood to get in and blow the two layers of the atrium apart. But it's a good point, and I do think pericardial... It's an almost pericardial tamponade, if it's not. Can I ask a question, or make a comment, and see what you think about your case? Because yeah, I've also been a little concerned. The newer catheters with the pressure sensing have a concave tip. And the older catheters without the pressure sensing had a convex tip. And I always felt like I could make the loop in the catheter safely and easily when it was convex because it floated right along with the wall. As soon as the concave tip came about with the pressure sensing, I always felt like we had the potential for undermining a plaque or something like that or undermining the right ventricular outflow wall, which I've had an experience with. So I think your point of maybe trying to make the curl on the iliac as the iliacs come together is a good point. Also, I think there was, I went to the booth, forgot the name, retrograde aortic, a retrograde approach that the sheaths take you into the LV with a pigtail. So I thought probably that could be another way. But I looked at this whole series of this case, the contact, actually the measured contact was normal and nothing like extremely high. So I agree with your point. Probably it's not measuring the friction. And maybe I should have shown this case, but I have perforated a left ventricle with a pressure sensing catheter with no evidence of any elevation of the pressure. And I think the mechanism of that, because before that happened, I started with that, no one can perforate the left ventricle. Before I did that, I think the mechanism is you get underneath the papillary muscle and you dissect along planes. And you can do that with a concave tip that's sort of sharp without the pressure registering very high. Well, I think that pap muscle area is a frequent region. Probably because there's traction with something pulling something up and then you've got a catheter this way. And that's why you've got reverse counterpressure. And we've seen that as well. Can I ask, is that okay? Yeah, absolutely. I have a question to Boris. I'm just wondering, it's very scary to see like hours later and the distance so far away and still have that complication. So after this case, do you still send the patient on the same day or do you keep them a little longer? No, fortunately, well, fortunately, in Germany, you have to keep the patients in the hospital for ideally two nights to get the full reimbursement. But many centers keep them at least one night. It is very uncommon in Germany to discharge the patient the day of the procedure. And it is our standard to keep them on the telemetry ward, despite the fact it's not a lethal arrhythmia, but still, we see early recurrences earlier, et cetera, et cetera. So yeah. Just wondering, any predictor that you can predict? It's so hard. It's difficult to predict from one single case. I mean, the other case that I showed to you, the gentleman with the proximal right coronary artery spasm after or during pentospinal ablation, he was interesting because this patient kept to have ST segment elevations on the ward the day after the procedure. So we treated him with oral nitrates, long-acting nitrates, and also calcium channel blockers. And it was discharged fine. And then we came back with atrial fibrillation recurrences months later. I don't know the exact time point anymore. But we ablated him again with thermal ablation. And he also had a coronary spasm. And I think that we diagnosed him with Prince Metal's angina. But that was a localized spasm, certainly. We don't know about the lady that deceased what really happened. Was it generalized? Was it just a localized spasm? But she was, before the event, she never had any symptoms of angina. Boris, I want to tag onto that because your story terrifies me because we are routinely doing St. Bay discharges. And it's like, how? Well, and we just had a consent, the statement come out on the heels of this meeting about St. Bay discharge. So are you based on this experience doing anything? Like, what are you doing differently? Like, because it's hard to know what happened. So hard to know then how to react? Yeah. I don't think, I cannot come up with, well, what we do differently certainly is we try to avoid delivering PFA to regions where we presumably have a closed coronary artery such as the upper mitral isthmus or such as the cavo-tricuspid isthmus. In very rare cases, we have done cavo-tricuspid isthmus ablation, but we preemptively treated the patients with nitroglycerin. So far, nothing happened. And we, at the PFA summit two days ago, Frank Cuoco presented data on 750 cases, and he never experienced such a terrible case. But I think we, I'm a little afraid that we deal in atrial esophageal fistula for coronary spasm with PFA, and it's certainly the only negative side effect that I'm aware of with PFA. I'm a big fan of PFA, but this is something we still need to investigate and understand better. Yeah. I will share an anecdote that's a little bit more uplifting, but it's not uplifting in the sense that it's like so great, but it's that we always implicate ourselves in any post-procedural complication. That's what we should do. It should always be, what did I do? How could I have caused this? But we had this one, I remember this one attorney that was coming in for an AFib ablation, and we were preparing everything. And obviously, we have a lot of patients, and sometimes we don't even remember when we've already done it, et cetera. And the nurse practitioner goes, you know that attorney? He had a massive stroke. And I was like, oh my God, you've got to be kidding me. And he goes, no, he's supposed to get the PVI tomorrow. And the point is, is it taught me that coincidences happen, disease happens. You know, in this case, it sounds like there wasn't routine CAD, but people get MIs. And could it just be that they're going to get something that actually happens in their natural history around the time of procedure? You never want to say that that's the first option. It's always us until proven otherwise, but things happen. And if it could have been just a little bit of a shift, then, you know, and if someone gets a fever, people would get the flu. But if they get a fever after a PVI, we did it, right? So there are coincidences that happen as well that sometimes don't implicate us. It's just important to understand. That's true. We have a question from the audience, yes, please. Please go ahead. Thank you. Rod, your emotional delivery was quite loud, and we appreciate that emotion. I think that we should be very humble. And whenever we finish, I think we think it's okay, but I think you need to be very straight with the patient that you don't know what the outcome will be until total recovery is going to be, and monitoring and not promising everything is okay. Well, everything may not be okay. So I think that, can you tell us, have you changed the way you talk to the patient or the way you deliver the message of possible complications? And have you changed your procedure? Yeah, I'm much more chicken-hearted. We had an epicardial debate today, and you can only take so much through your career, but when you're young, you haven't had the trauma. But what happens is when you've had enough trauma and you haven't had to open people up surgically, yeah, it's four or five. I keep a list of all my complications on my phone. That's another thing I do. And it's confidential, et cetera. It's all encoded and encrypted, but the point is I don't want to forget a single one. I don't want to forget a single one and underestimate, because you always ask someone, how many of you have had these? They say, I haven't had that many. And I look at the list, and I go, oh, I forgot that one. And I think that's really good, to keep yourself in check. And I do think that every time I go and I pull the curtain, I remind myself, this could be the name that makes me almost want to leave medicine, that every single patient, whether it's a generator change or whatever, this has to be taken care of. It's not just a gen change. It's not just a PVI. This one can break you, and I think that humility is important. Any of the fellows, I think Zenith, every time I leave, at the end of the day, I say, today was a great day, because nothing terrible happened. There's got to be some gratitude, because you would just say, well, I just did three PVIs. It's fine. Yeah, but that could be three open chests. That could be three sudden deaths, and every one you just have to celebrate and be grateful for, but just remind yourself. So there's a spiritual journey that comes with this, and I'm sure it resonates with everyone, because if you just harm one person in your life, that's not what we're here to do. It's just even one person causing harm is heartbreaking. Absolutely. I just want to point out, we're doing stuff that is not going to necessarily kill the patient for the most part. We end up with death in a patient that walked into the office, for the most part, fine, and we end up with a disaster, such as a disaster that we describe. It's rare, but it's devastating, and I usually tell the patient, I do not walk on water. We're just human, just like you, and we do the best we can, and we'll monitor very closely and very carefully. We'll do the best we can, and we hope for the best. That's all we can do. Thank you. Let me actually make one other thing that I think is an important principle, and that is the incident, the complication is one thing, but I've seen more people get into trouble from lack of recognition of the complication and inappropriate management of the complication. We had that with atrial esophageal fistulas. The people in the clinic get a call that someone has fever 10 days after a PVI, and they say, well, take some aspirin and get a urinalysis and make sure you don't have a UTI, and we had to teach them very forcefully that we can't miss a complication. So I think many times the complication is much worsened by the management that comes afterward, and your staff has to be trained to pick those things up. Thank you again for sharing these wonderful lessons for us all to learn, and I think everybody should attend this session, because you go around, you see all the heroic things that are being done. You're just like, okay, I'm just going to do it. That kind of brings you and humbles you down. I think it's really, really important. So again, thank you for sharing this. A quick question about this. I agree with Dr. Zhu that Boris, my friend, that really, you know, we have to think what we're doing with the PFA case, and I know we probably will never know what is the cause, but if you think there is a spasm, the immediate action would be worse, right? Because the spasm would leave, and then later you didn't have anything. This happened way later. So it's hard to blame it on spasm. Don't you think so? I'm just thinking. I don't know if there is. I really have no idea. Any thoughts? I know you gave it a lot of thought, but this is just, we do this all the time. I mean, we play around, maybe mitral isthmus all the time. I don't touch the trachea with that, but it keeps you thinking. It's certainly debatable, and I don't know the exact answer. The only thing why I think it was a spasm is that she didn't have any evidence of plagues, no plague rupture, nothing in the right coronary artery, also not on the left side. She did not have any thrombus material in the coronaries during orthopsy. And there are these other cases, as I showed to you during the presentation, Dr. Luther's case from the UK, where they did coronary angiogram in this acute situation, and they found the spasm. That was 45 minutes later, but still, remote from the energy applications. And I would guess that this is the best explanation. Or massive air that accumulated and then remobilized because it's in the RCA territory, you know, and it's that remote. But it could be a massive air embolism from a sheath exchange or something that was late, but we'll never know. Yeah, but there were, well, if, yeah. You mean, and where, would you think that the air collected until, like, seven hours later? Yeah, like, somewhere in the left atrium, it filtered around, and then somehow there's one big bolus of it, but, you know, hard to say. Well, along those lines, too, there's a couple of questions. Spasm five hours later is weird, too. They're all weird. A couple of questions came in related to this vasospasm question in treatment. Like, just like we were giving PPIs routinely to prevent atrioesophageal injury, you know, should we be starting nitrates in people prophylactically, calcium channel blockers, for a period of time? Yeah, it's a good question. We don't know the answer. I asked the same question during the PFA summit, and there was a controversial discussion around this, maybe long-acting nitrates as a prophylactic measure for all PFA ablation. It's going to be difficult to prove benefit. I think, to the best of my knowledge, until today, PPIs have not proven any benefit to prevent atrioesophageal fistula. No, exactly, but we continue to do it. We do. We just do it because there are no side effects. It might be different with all nitrates. Right. So, yeah, I don't know. Melanie? Hi. I just wanted to comment on this, and I think that giving a treatment without knowing what to treat and what is actually the cause of it, and I think what you can kind of learn from this lesson is that there are some of the complications that seem just to happen, right? Like, you did everything the right way, and it just appears, and you don't know how to get out on the other side and how to do it better next time, but the case with the potential spasm, it actually can make us more aware that we need better research in this regard, and we know that the spasm thing is much more complex, right? We have the proximity-related ones that we think they are due to the electrical field that's close to the vessel, and then we also have two types of damages. We have the spasm itself, but we also have maybe some intimal injury that we cause to the artery, and then there are those spasms that have timely delay that we pick up from case reports that have been there, and then there's generalized spasm, and I think there's a lot we don't understand. We don't know if it's the autonevus nervous system. Does it have to do with hemolysis? Because cells are being disrupted, and we release substances there, so I think this case at least should drive research and also force industry to pick this up and find solutions to the problem. That's a great comment. I guess just a kind of discussion amongst the panel. I guess in Germany they don't do same-day discharges, but I don't know, Kyoko, Bill, Harris, are there procedures in which you are doing this routinely for ablation or none at all? You mean the post-procedure? Yeah, same-day discharge. No, we don't do the same-day discharge. We usually stay overnight, and after hearing all the story, I think I may keep longer. You could argue we didn't rescue the patient. Yes, exactly. We've done same-day discharge since 2016, since we moved to cryo and then to this with vascular access closure and things, and several large series that have shown no harm, no signal of harm doing that from Britain, one from Australia. I think it's very sobering, obviously, because we don't know how to identify the at-risk group. This is such a delayed event, seven hours afterwards, and most of our people have gone home at sort of five, six hours, something like that. If the groin's okay, the echo's okay, so it's a very hard question. Also, I find it like the PFA devices or cryo, I mean, it's a one-shot device, but I think the system becomes so bulky, so I think we really have to train the fellows how to prepare the sheets and take out the air, so that's another important thing. Well, we're split. I've done this for 43 years, and I've been resistant to same-day discharge. You don't pick up a lot that overnight till the next morning, but if you do pick up something, it's important. A night in our emergency, having to come into our emergency room at night is awful, and they may not pick up the complication, and so my younger people like to try to get them out. I get them out if they want to get out, if they're pushing, but I still like to keep them overnight, especially if they live more than 15, 20 minutes away. Just a question for Kiyoko especially, but in light of the TRAVERSE trial, I had the chance to speak to Greg Marcus about this yesterday. I think the arguments in favour of moving to a predominantly transeptal approach for most things that we do becomes compelling, even if you leave, just from the brain point of view, even if you leave the A-order out of it, and I know for a fact Rod's not with us anymore, but Rod did some cases in TRAVERSE of outflow tracts transeptally, so given enough will, you can get most places transeptal. What are your thoughts on that? Yeah, because I was trained by Bill, like a retrograde, it's easier for me to do that, but I think we usually use both, especially a patient who doesn't have too much atelosclerosis and without any aortic elongation, but I don't know. Maybe the system I just saw in the booth probably would be a big help. We often will use a long sheath anyway for going retrograde, but I almost never go retrograde unless I think I have to be above the valve for some reason. On the cusp, probably the cusp ablation. Yes, that's right. Okay, well I think, I again want to thank the speakers for their humility and expertise and excellent deliveries and grace, and thank you all for staying.

ablation complications

atrial fibrillation

intramural hematoma

pulse field ablation

coronary spasm

ventricular pseudoaneurysm

electrophysiology

iatrogenic trauma

patient outcomes

vascular injuries