So, mine's a little bit of an overlap, because heart failure doesn't exist by itself, as we talked about yesterday. And it may be very simplistic at the same time, but I'm hoping that – does this work? Not work? Sorry. Perfect. Okay. So, and I don't know what we mean by rapid fire, but deliberation certainly we can deliberate, because there are many ways to approach the same case, and none of them are the wrong or the right way, and you'll see that in two seconds. So, this is a 58-year-old gentleman, five-year history of non-ischemic cardiomyopathy, had a single-chamber ICD implanted, because the ejection fraction was around 34 percent, okay? Was NYHA Class 2, and we talked about the NYHA yesterday, and on an optimal medical regimen. So, one of the first questions people ask is, is the patient on an optimal medical regimen? And yes, this patient was on an optimal medical regimen. He had ACE inhibitors, Coreg, and diuretics. In the future, when we look at optimal medical regimens, you'll also have neprilysin inhibitors and SGLT2 inhibitors coming down the pike, so be aware of that, too, as we talked about yesterday. So, two and a half years ago, this patient with heart failure develops prognosomal atrial fibrillation, okay? Patient – as we talked about yesterday, again, about 20 percent of patients, 25 percent of patients may not feel their atrial fibrillation. So, here you had a patient with heart failure, now has AFib, and manifests for the first time admitted with heart failure, so a straight-off admission out here. So, start of the patient felt that, you know, we need to control this AFib, and we started the patient on ticosin or defedolide. So, there's a whole – there are many antiarrhythmics that you can potentially use in heart failure, but the ones that have been studied effectively are defedolide, and there's something called a Diamond CHF study or a Diamond HF study that showed that defedolide in patients with a depressed ejection fraction actually improves outcomes and can control atrial fibrillation, all right? So, with that, there was a reduction in burden of the atrial fibrillation for six months, but then subsequently, there were recurrences and decompensation, and the patient then got admitted again for heart failure and needed a cardioversion again, all right? Repeat echo showed that the ejection fraction, which was 34%, was now 30% within the error of variability, plus, minus five, but certainly was trending in the wrong direction. There was some LV dilatation, too. Point out here is the left atrium in this patient had, over time, remodeled, and it was dilated, and it was about 47 millimeters in the anterior-posterior diameter. Normal is four centimeters and less. That's the average. Obviously, we need to be able to individualize that for body surface area and index, and we do use those now, but at that point in time, we just had the measurements, so it's important also to kind of put that into context. Had a normal heart otherwise, there was mild mitral regurgitation, mildly elevated pulmonary artery pressures, which you could expect with patients who have longstanding heart failure. There are elevated pulmonary pressures, and they can be mildly elevated. When they get elevated, another thing to kind of keep in mind, you can have remodeling of the right atrium, and sometimes that can confound the arrhythmias that these patients can present with. But nevertheless, when we saw the patient, the patient was in normal sinus rhythm, had been converted, was already on defedalide, the QTC interval, which you know, all you know that we monitor the QTC interval in these patients because it's a class three antiarrhythmic, so it's a potassium channel blocker, and potassium channel blockers can actually prolong the QT interval, and that can actually enhance the risk for having other arrhythmias like torsad or ventricular arrhythmias. So that was fairly normal in this particular patient, and all the other laboratory tests were reasonable. So my question to the panel. What would you do? And you know, this is again, there's no right answer out here. You can slice and dice, or as they say, skin the cat in many ways. So the question is, patient with heart failure, presents with AFib, tried multiple medications a couple of times, has been cardioverted, will we now just go snip the AV node with an ablation and upgrade the device with the CRT? Or would we say, okay, you know what? Rhythm control did not work. Let's take a step back and rate control this patient, and let's see how this patient does with rate control. Our third strategy is, all right, there's one other medication we haven't tried. That's a heavy hitter. That's amiodarone. And everybody recognizes amiodarone is a sodium, potassium, calcium beta channel blocker. So it's like a cannon. Can have long-term potential side effects, but can we actually try amiodarone instead of defetalide and see how the patient does? Go ahead. Just a clarification, on your last slide, you said the patient was in sinus rhythm, but by your questioning, you make it sound like he's having recurrent AFib? Correct. Okay. Correct. Correct. So at this point in time, when the point of assessment was done, this patient was back in the hospital in sinus rhythm, cardioverted, but knowing that he's already had more than a few, there's a high likelihood that the defetalide is not working, do we switch it to amiodarone? Or do we just take off the defetalide at that point in time and say, okay, now let's put some rate controlling agents on board to control the rate in case the patient goes back into AFib, knowing that an antiarrhythmic is not working. Remember, this patient is 50 years old. Okay. Want to put that into the equation out there. Or do we go for a catheter ablation of AFib in a patient whose left atrium is about 47 millimeters and has a history of heart failure? So many ways to slice and dice that. David, did you want to kind of take a pot shot how you want to approach this? Yeah. So a younger guy, I'm not a fan of amiodarone because of the small but definite toxicity risk that's cumulative over time. This is a patient that sort of fits perfectly into the CASEL-AF trial demographic. And as we know, as I discussed yesterday, that trial showed actual mortality benefit with AFib ablation in a heart failure population. We also know that for, you know, probably a number of different mechanisms, people do show improvement in LV ejection fraction after catheter ablation. Not an ideal ablation candidate because the patient has persistent AFib and some LA enlargement, which tells me that they have a myopathic atrium and pulmonary vein isolation alone may not be enough, but that's certainly where I would start. So I think that's a, you know, a straightforward thing to do. Younger guy, I would certainly offer that to him. Rod, go ahead. Yeah, I would agree. I think that there are two things that I'm hoping to achieve. One is, you know, to improve symptoms and keep them at a heart failure. And then theoretically, can we get the ejection fraction a little higher? There may be a role of MR here, right? If there's fibrosis, maybe we're not going to get that improvement in the F, but we may still have that other benefit. But I would certainly counsel the patient this is going to probably take more than one ablation. We may start with PBI alone, then move on to a second, and ultimately may require some surgical approach if multiple ablations plus drugs don't do the trick. Shiv? I concur with that. We would aggressively try to do what we can to reestablish sinus rhythm. It's going to take more than one procedure, but that's definitely worth the effort. Susan? Agree. Agree. So everybody on the same page. So I hope, I hope that I was on the same page, too, out here, because otherwise I'd be chastised. So we decided to go down the ablation route. So what would your ablation strategy in a patient with heart failure be? Would you say, would I just do a pulmonary vein isolation out here? Would I do a pulmonary vein isolation with a posterior wall isolation? Or would I also say, hey, this patient has a remodeled left atrium. There's a high risk that this patient is going to come back for other ablations later on in the future. Let me take out everything. Let me do a roof line, a posterior line, a mitral isthmus line. Or do you want to go after complex fractionated atrial electrograms, which, again, is a historical perspective to ablation? So let's start from the other side. Susan? I think, as the other panelists intimated, I think we have to lay the crepe and let the patient know there's a high risk of recurrence, high risk for a second ablation. But I think it's reasonable to start just with PVI. He still paroxys. Oh, no. You had to cardiovert him. He cardioverted him. Yeah. You cardioverted him. So I would still start with PVI. We just don't have enough data to say doing all that from the beginning isn't going to end up giving him a lot of benefit. Sounds great. Yeah? Look, there are additional subtle modulators of this. We would look at the MRI. We'd make a few more additional decisions. But perhaps we would tend to sort of be between options A and B. We know that we will not do D, because that is meaningless. And it's probably going to be prorythmic, because you'll end up with more problems. And we'll definitely stay away from C, because that can also be prorythmic if you create a root line and the patient may have done well. And now you've essentially committed the patient to potentially a worsened heart failure episode of depressant with a catheter-induced prorythmic atrial tachycardia. Can you explain to the folks out here what you mean by prorythmia with CFE and with lines? Thank you for stopping me for the jargon. So we don't talk about this as often as we should. But when you actually do ablative lesions in the heart, think about this. You're treating a scar-based problem by making more scar. So you better have a good reason to make the scars at the right spots. And all technologies have limitations. So when you make these ablative lesions, the more and more you add on to a procedure, it's very hard to actually come up with endpoints and verify what you've done. So if you make a line of lesions, there are gaps in that line. It may play dead for a little bit during ablation. But then if those areas start conducting again, they don't conduct normally, they conduct a little slowly. So that is like planting a seed for a future arrhythmia, one which the patient would have never had. So we joke about this by calling this, you know, iatrogenesis imperfecta, iatrogenesis perfecta. And of course, sadly, there is iatrogenicide in that entire sequence. So the surgeons do iatrogenesis perfecta when they do a bad MACE procedure. And this would be iatrogenesis imperfecta because you're setting the stage for something bad, which really should be avoided if you can. Rod? Yeah. This is what we struggle with. I mean, I think that there's pretty good data that, you know, for example, we use a lot of cryo-balloon. You know, maybe even for persistent AFib, you get success rates of 50 to 55 percent. It's hard to predict up front which half you're going to get. But then if you need to take the patient back, I think that, you know, you've taken out 70 to 80 percent of the posterior wall already, and it'll make your job that much easier. And I would aim towards doing less. Now, I would ask the panel and ask you, what if you did a voltage map and there was scar all over the posterior wall? Would that change your mind to say, hey, this is not just a PV problem. This is a more diffuse problem. And would you sort of change your opinion? I know I'm on the panel, but let me throw that back to you. Totally. Totally. So, the reason for a voltage map showing that there's a lot of scar in the posterior wall kind of suggests that there are many other areas potentially as triggers and re-entrant strategies for actually AFib, you know, surfacing again. So, if I do a voltage map, which I usually do in every case, I don't know if I did one out here, but I'll tell you, but then isolating the pulmonary veins may not be the entire solution. Now, in those situations, I personally have a low propensity of actually taking out the posterior wall in those patients. I don't do mitalissimus lines at a first pass ever, unless they've manifested the atypical flutter, which was their clinical flutter that they presented with. But I will take out the posterior wall in a substantially remodeled left atrium that has fibrosis. But if not, I am a minimalist, and I prefer to just do a pulmonary vein isolation. David, do you have thoughts on that, or? Yes. Yes. It's time for the next case. Thank you.

heart failure

atrial fibrillation

ablation

medication

catheter ablation