Okay, thank you so much. So let me jump into this case, 48-year-old male, NYHA Class III, symptomatic PBCs for a decade, EF shows 25%, nuclear stress test was negative, the patient didn't, the workup didn't involve a CT or a coronary imaging, the PBC burden is 35%, MRI and PET are normal. So quick rapid fire from the panel, and I'll give you the ECG because you're going to ask for that anyway, so, and I'm also setting it up because the ECG that was obtained in the cath lab, right off, would anyone not take this patient to the cath lab? After this workup, I'm sort of leading the panel by the nose. Yeah, I mean, there's a lot of PBCs, you know, 35%. But a comment about the workup, because we've been criticized for being, you know, throwing the book at them, you know, trying to get every possible workup, and I can of course defend our rationale as to why we did this, because it's a relatively young patient, and using the Passman criteria, anyone who is within a decade of our age group is relatively young. So, so there you go, right up there, and I said we have to do the full court press, and it meets just, even just based on the burden of PBCs, but we sort of went the extra mile to look at coronary workup. The biggest challenge here was getting a PET, so let me actually ask the panel what your take on that is, because as electrophysiologists, this is a little bit of a intellectual, intriguing, hot button issue, in fact, one that reduced a less number of ablations, so, so any comments on whether, when you would time a PET scan? So I think all of us would look at an MRI and say there's no scar, so you think it's tachy-induced myopathy. Could you just describe to the audience what a PET scan is and why we do it? Sure, okay, thank you for stopping me on that. So I'll tell you why we do each one of these tests. Lots of PBCs is a bad thing, which means we think PBCs itself could be depressing the heart's function, and as shown by the echocardiogram. Stress test is to make sure that there's no coronary arterial disease, which, if you've had a previous infarction or something, that can drive your EF down, and of course it impacts medications we use and so forth. And the burden of PBCs is also another strong driver to say that this is potentially the problem. Later, we have to find out if the PBCs are coming from one source or multiple sources, but what I didn't put over there is they're all monomorphic. They were coming from one source. We do an MRI to make sure that there's no scar. Sometimes people have a scar, they've had myocarditis that they didn't know about. So that is good. So now it's really looking like this may be, PBC may be driving this. But as a group, we were a little more biased. We constantly searched for reasons as to why a given region of the heart should actually cause those abnormal beats. And we had a huge, and we still are, on a given day, we tend to lose this fight quite a bit with payers. We get the PET CT scan because it actually is used, in this case, to identify areas of the heart that are inflamed. So this is to search for inflammation, and we and other groups have actually found areas of the heart that show spots of inflammation, which actually is the source of those PBCs. So when we see a funny-looking PBC, which shouldn't come from the typical region, which is the outflow tract on the aorta and the right ventricular outflow tract, we often wonder why should that area of the heart misbehave, right? So that's why we did the PET CT. It's a bit of an overkill. I'd be the first one to tell you this, but in a little over 200 cases where we fought for this, we actually were able to identify causes where we treated the patients with a short duration of anti-inflammatory drugs. But this is a big unmet need for us in the field. People say, oh, you love VT ablation. Why are you doing these things that actually reduce the total number of VT ablations? But it's great if you can actually prevent a patient's heart from getting inflamed. So just quick rapid fire to know when you would order a PET, because it's not agreed in the field. So we overdo it up front. Yeah. We mostly use PETs to look for sarcoid, which is out there and is on the short list if a patient who's been pretty normal suddenly shows up with lots of non-sustained VT. That's frequently the finding, or high density PVCs. We don't routinely do it to look for magical little inflammatory spots. And you're saying that when you've identified those, there have been no findings on T2MRImaging? So T2MRImaging is a way of looking for edema and inflammation specifically in MRI. And head-to-head comparisons have not been done. In our experience initially, we didn't have good T1, T2 sequences. We have a very sophisticated MRI group. So we've been now, in the past three years, we've actually done the side-to-side comparison so that we don't miss inflammation. So we call them arrhythmogenic inflammatory cardiomyopathy if we just see spots of inflammation. And there's a new paper that has come out in Circa-E. This is from the Kansas City group, Dr. Lacherty's group. They actually did a multi-center study of what we retrospectively showed. So there is going to be a subgroup. We have no idea whether it's 5%, 10%, or 20%. Our referral base is, of course, very skewed because people have already referred to us exclusively for VT ablation, and we went around searching for it. So it may be an enriched population. I'm just curious, you know, if someone has a PVC somewhere along the way, some of these idiopathic cardiomyopathies may very well be inflammation-based. And one of the most exciting calls that we received after publishing our paper in Heart Rhythm on de novo use of PET scans for identifying PVCs came from NHS in England. And you often identify them with people who try every possible way not to pay for things. And they were looking into actually hiring for FPG PETs, which typically is used only for cancer patients, but it's a big picture of medicine. So that's a great answer, Dave. So Rod, Susan, quick, rapid-fire, when you'd get a PET CT? I don't know that we order routinely for patients with PVCs, but a non-ischemic who has, you know, recurrent ventricular tachycardia, I think our threshold is getting lower, so it's easier to order them at our facility. Andrea and then Jack. Same as David said, the hemorrhage, and then you may be in the lab, and you talk about whether I get scarred in the face. I have to tell you, you know, when I was in med school, we thought there was a certificate on sarcoid, and we would never consider it in, you know, older people. Sure enough, I'm finding it a lot more than I ever expected. And it's cardiac only, too, you know. Typically people, all these things we read in textbooks, our patients don't read the same textbooks. So therein lies the problem. Jack, do you want to make a quick comment? Yeah, no, you know, I wouldn't rush to doing a PET CT or FTG for sarcoidosis. I'd probably, if I was suspecting sarcoid, I'd probably do a chest CT, look for pulmonary extracardiac sarcoidosis, then go in for an FTG PET. But I would start off with the MRI, and if there's nothing on the MRI, then I would decide, again, whether I'd come down, whether I'd go down an antiarrhythmic route first or an ablation route first. So, again, since I'm doing this after the fact, I can always present the case in a certain way, where we can, this is Hollywood, you can cut the movie and show the movie the way you want. So the reason we actually really pushed for the PET is because we looked at this 12-lead and we said, OMG, this is going to be a very long day in the lab. So, and maybe rapid fire, since I have five more minutes, but rapid fire, one comment, anyone from the panel to make a very quick comment on this ECG, because this is the kind of ECG that makes your heart stop. So, a quick comment from anyone on the panel, whoever wants to take it, for the benefit of the audience, and all the measurements are there. And while one of the panelists are going to comment, I'll tell you what really catches your attention in this PVC, which of course is a huge number of it, is the time it takes for the cumerus to reach its very peak. And when you look at these measurements, this tells you that this is coming from a tough location in the heart. This is not going to be something that you can easily access with your capita, either on the inside or the outside of the heart. So, any one quick comment from the panel, would you agree? Exactly. So, the area that we're talking about is the summit. And in fact, this is a very tricky neighborhood in the heart. And there are many options. The reason is, this particular area, this comes from the famous McAlpine collection, which we are now restoring for the field. So, this is a beautiful section of the heart showing you the LV, the origin of the aorta, and the region from which this PVC is coming is right here. So, and it turns out, this area is also covered by a lot of epicardial fat. And, so this is the sort of the denouement, the final question for the audience in a quick, rapid fire. There are multiple approaches that can be used, and maybe the audience, the panel can make very quick comments of how they would approach this. And each one of this has, of course, had data sets and the sequence of how we would go about doing it. And I'll tell you what we actually did for this patient as the concluding slide. Any quick comments from anyone in the panel? Again, we're putting up not just a rare one-off case, but these are becoming more and more common. So, these six approaches on any given week you come, there's going to be some combination of this that's going to be done because we are going all the way out when you see PVCs, especially which we think is causing heart failure. So, this is one of the little frontiers of VT ablation where the time and effort and the radiation we take and expose ourselves and the patients to is worth it because you can prevent the heart from getting worse. So, I'd first, obviously, offer this patient Xylitine or something, kind of see if the antirethnic reduces the burden. Even if it reduces the burden, it would improve the ejection fraction to some extent, would make the invasive procedure at a later date a little more safer, which is, you know, you have a better EF and you can do a better procedure. You know, and knowing that it's epicardial, but I would still preferentially go in, map transeptally, go retrograde if I need to. I'd first go into the coronary venous sinus and actually go as anterior as possible and see if you can map it from there. Sometimes you get lucky. And sometimes, obviously, it's dangerous to ablate out there too because you're in close proximity of the coronary arteries. But I would actually do everything at the same time. That is, go endocardially, map the coronary sinus, and then go retrograde if I don't get anything from there. And then decide epicardial at a separate setting or the same setting. That's, again, something, you know, you can make that decision before talking to the patient. I completely concur. Rob, David, any quick comments? Well, you know, I think sometimes it's the chicken and the egg situation. You don't know whether the low EF caused the PBCs or the PBCs caused the low EF. So I agree. Apply a drug, try a drug first, knock the PBC burden down, reevaluate the ejection fraction. If it doesn't get better and the patient has no symptoms from the PBCs, well, then what's the indication? Yeah, I think that's well taken. And as it turns out, that one piece of information on this patient is the patient didn't tolerate meds well. I didn't want to make it a little novel when I did a five-minute case. But that point is well taken. And nobody really knows what the time window of repeat echo should be. But that's perfectly reasonable to do this because you don't have a scar. It's not inflamed. So then if you can reduce it, you know for a fact that it's well worth the effort to doing this. So one quick comment to follow up on Dr. Singh's comment is percutaneous epicardial mapping really is not very useful for these cases because most of these structures are hidden under epicardial fat. So you map from within the venous system. And the last point over here, what we actually did in this case was we mapped all those approaches. But we were able to avoid surgery by using various approaches where we mapped within the coronary arteries. So this is actually a neurointerventional coil embolization wire that you can put into arteries. This particular patient, that couldn't work. And what we ended up doing was we actually, this is where it's actually useful to talk to other colleagues in interventional cardiology. And we actually use the Stingray system that is made by Boston Scientific, which is a coronary CTO system where you can intentionally dissect out of a coronary artery shown over here. And you can just stick the wire into the myocardium and ablate it by delivering RF. So this is a chronic total occlusion system. Again, all these approaches can be done logically. And it's centered on anatomy. It's centered on technology. And in this case, we just used the ablation catheter and touched the RF wire. And we were able to ablate intramyocardially. So that was what was done. And the patient has done well. And I'm going to stop here on time. Thank you so much.

premature ventricular contractions

low ejection fraction

echocardiogram

PET scan

ablation catheter