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EP on EP Episode 76: Intersection of EP and CHF wi ...
Eric N. Prystowsky, MD, FHRS, sits down with Silvi ...
Eric N. Prystowsky, MD, FHRS, sits down with Silvia G Priori, MD, PhD, to discuss gene therapy for the treatment of catecholaminergic polymorphic ventricular tachycardia (CPVT).
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Video Transcription
♪ ♪ Hi, this is Eric Vrstovsky and welcome to another segment of EP on EP. What a real delight it is for me today to be interviewing my friend for many years, Clyde Yancy, who is currently the chief of cardiology at Northwestern Medicine and holds a bunch of other hats, such as past president of American Heart and a enjoyer of wonderful wines. So, Clyde, we will have that glass of wine one day. Clyde, welcome to the show. I'm delighted to be on the show, but this should be EP on heart failure, not EP on EP, unless my membership in HRS qualifies me as being an electrophysiologist, but I'm really delighted to visit with you. I've learned so much from you over the years and enjoyed our discussions so very much. So thank you, Eric. Thank you. It's my pleasure. You always have my membership for you in the EP society, so don't worry about it. What we're going to talk about today is an area that you and I have discussed in the past, and I think it's really prescient because we're getting into a lot of overlaps in arrhythmias and heart failure and how to co-manage them. So, Clyde, let me start off by just asking you, what do you think some of the major issues are in dealing with arrhythmias and heart failure in the two sort of silos? What are your thoughts? So, Eric, I really love that you use the word prescient because it gives us a license to think about where we're going. I mean, we all know the history, and that's all good. But when we think about where we're going, we begin to understand this phenomenon of the intersectionality of heart disease in general, as I see it, but specifically heart failure and arrhythmias. So, case in point, if you think about risk factors for atrial fibrillation, boy, they sure line up really well with risk factors for heart failure. So even if we start at the beginning of the cascade, how do we prevent heart disease? As we think about preventing heart failure, Eric, we're also thinking about preventing AF. So to be very succinct in an answer to your question, the prescient nature of this conversation is that everything we do for prevention, treatment, disease management, even end-of-life care, really does overlap and intersect. We haven't treated it as such up until now. But I think the pivot, the inflection point that we've reached is that it's not necessary for our respective disciplines to come together and realize how much culinarity there is in what we do and how we think. So let's take a couple of examples that are everyday problems that I think you and I work on together. Let's start with the elephant in the room, atrial fib. And it has multiple areas. One would be some of, sort of, you've talked about in the past, randomized trials. There are randomized trials in AFib. There are tons of randomized trials in heart failure. You've been one of the leaders in all the areas in RCPs. What are we missing with AFib? When I see a patient with AFib and there may be some decrease in ejection fraction, how should our buddy system work? What should we be doing together to get the patient to the right place? You know, Eric, one of the things I love, absolutely love, is that every effective therapy that we use for atrial fib management or heart failure began with a question at the bedside. Why is this happening? Why is this occurrence as it is? Why is this patient not responding? What hasn't happened is that our respective disciplines haven't come together and generated a mutual question. Because if we did that process, just that one alignment, then we would have the impetus for the kinds of studies that we would like to see. Meaning, let's enroll a population with heart failure and atrial fibrillation. I know there have been efforts to do this before, so I really want to applaud those who've done some really remarkable trials in the past. But we need to answer more questions. We need definitive proof for AFiblation. We need to understand precisely how high is the risk for stroke? Is there a group that is at lower risk? There are many things that we need to understand. The latter because there's already so much polypharmacy in the treatment of heart failure. Is there a patient with heart failure who actually doesn't have the same risk? Eric, think about when the calibration for the CHAS-BAS2 score was created with heart failure included. Heart failure then was a very different condition than it is now. Does it still need to carry the same weight, perhaps? But these questions are important going forward. So I think coming together, particularly if we're starting with AF, thinking about this jointly, not just about AF, not just about heart failure, but coming together and think about this as the patient would want us to consider this. The patient wants us to say, for a patient like me, what works? And if me means I have both heart failure and atrial fibrillation, we need more of those data points available. And I totally agree. There have been some very nice studies done by Dr. Packer and Maroosh and a few others. But you're right. They aren't getting it. I know the question that you're talking about. Until those studies are done, let's take a patient. You and I are both clinicians. We don't just write papers or guidelines. You and I have been doctors for a long time. I know I'm older, so I give you that. A little bit. So it's not uncommon that I'll have a patient that I'll see who has what I feel is a tachymyopathy from AFib. And I almost always will co-manage it with one of my heart failure buddies. One of the things we come up with all the time, we argue over, once we get them under control and the EF has gotten to a good level, sometimes normalized, do I need to keep them on all the heart failure drugs? And especially if they started from heart failure and then referred to me, because there's no chance that I'm going to stop a heart failure doctor's drugs without losing my hand. So what are your thoughts on that? I mean, we don't have those studies, do we? So use that model and change the prism. Because what we would like to understand is, what are the risk factors for developing a tachycardic-mediated cardiomyopathy? Is it age? Is it pre-existing subclinical coronary disease? Is there a genetic predisposition? Who's at risk for this? Second, what's the dose? How much tachycardia is required before you see the LV dysfunction? These are the kinds of questions we'd like to have answered because it really informs immediacy. Is this something that we do right away? Is this something that we say, let's treat the heart failure first and let the heart rate settle down on its own? Having those kinds of foundational answers, foundational meaning they get to the path of physiology, helps us. And that's, again, back to this point of, how do we manage this obvious intersectionality that helps us realize that both of the disease processes that we respect would end up doing substantially better if each one informed the other with new provocative hypotheses and we did the right trials. I'm just going to bring up one other topic, which is ICDs, which is the topic you and I could discuss at nauseam. But I will tell you, I'm going to lay out a statement and let you respond to it. How's that? That's a good approach. Many, many years ago, I looked at our own group at why we weren't putting in more ICDs with class 1A indications. Now, the heart failure community, above any, has been studying things in an RCT. So when they get a class 1A indication, most of the people certainly follow that indication. And I was really disturbed that we had so many people I found just doing a bit of a search of my own group, that were not even approached by anyone, even though they met criteria for class 1A ICD preventative therapy. And I realized it was a huge bias against it. And that was shown, get with the guidelines, there are all these things that I'm not involved in, but I know you've been involved in, showing even less than 30% in many places, penetrance of class 1A. A lot of these people were probably managed initially and mostly by heart failure experts, right? Because they have heart failure and low EFs. They don't come to me unless they're sent to me. So explain that to me. What am I missing there? So you're missing a couple of things. The first thing is that the vast majority of heart failure in this country, the vast majority, is cared for not by heart failure physicians, not even by cardiologists. It's cared for by primary care physicians and internists, and they oftentimes do an incredibly credible job. So we have to understand that there are very different constituencies involved in taking care of this patient population. But the next thing we have to understand, and it's a sobering message for those of us that are involved in original clinical science, we do the trial, highly qualified. We have inclusion criteria, exclusion criteria. We come up with a finding, a finding that sometimes requires some effort to interpret. There's some nuance in how the study was executed, and there is some uncertainty still in the findings. But nevertheless, the FDA reviews it, adjudicates it, and says, we agree with the indication. And then the guideline writing committees say, we agree with the indication. But the real critical test is what happens in the community. When we see prescription hesitancy or referral hesitancy, there are lots of reasons for that, but at least some of that, Eric, is because there are physicians that still are at equiposte about things that we believe are evidence-based because we have intimate knowledge of the data, but our intimate knowledge also informs the groups who are not studied, on the groups in whom there's not an indication. I would submit to you that the daily busy practitioner seeing 30-plus patients day after day has no time to think about all the experimentations and is trying to understand, you know, is this the candidate or not? And so, you know, I think we have to work very carefully to understand how best to deliver the message. So let me just tell you one more thing. Sure. Even for those of us that are well-informed, you bring up the ICD, do you really know, do I really know, which patient truly benefits? Even now, let me get you to really digest this. I was one of the SCUD-HeF investigators. We released those data in 2005. Today, we still have no better predictor of who responds to the presence of an ICD than injection fraction. And even following that response, 85% of those ICDs never offer a definitive therapy. Now, recently, we've had reason to believe that there may be some ways we can calibrate that decision better. But even for those of us that are facile with the information, we have to acknowledge that that's a very crude indication. Everybody with a little bit of evidence can get one of these. I would totally agree that, I would never make that comment, you know me, that everyone needs it. But I'll tell you an interesting thing. I was at a meeting with, I know you know Dan Marks. Of course. A fellow Dukie, friend of mine, another Dukie. I know you guys who aren't Dukies and just don't like that. But at any rate, a fellow Dukie who was at a meeting once and said something that I always remember because it's remarkably simple but telling. He said, ICDs are one of the few therapies we have, we give people, that we can tell you when it wasn't necessary. So we give people statins, beta-blockers, we give people all those things. But we really don't know in the same token in the drug world, was that person really helped with the statin? Maybe, maybe not. But when an ICD doesn't go off for a year, you can say, oh look, over this past year they didn't need the ICD. But when someone doesn't have an MI in the next year, can I really say it's because of the statin I gave them? We both know you can't. I thought that was a remarkably insightful comment and I thought about it a lot and I think that's part of the problem. It is, we know not every ICD is necessary. I agree with you. I totally agree with what you're saying, Clyde. The problem is I don't know how to figure that out. So, and I'm not Solomon and I don't know how to figure which one. And I would be the first to tell you our ability to do that is not very good. Although, as you know, I'm a huge fan of CMR and I've been using that a lot in my own practice. But still, I agree. But just think about that comment. It's pretty interesting, right? When an ICD does inquire, we know for that year it wasn't needed. So think about this. One of the marks of genius is simplicity. And Danmark disqualifies. But if we try to think about what are the takeaways here, it's precisely what we've been discussing for the last several minutes. We can't pretend as if we have a sufficient database at present to really answer all of the questions or deal with all the clinical scenarios. That's why we must be relentless in our derivation of new hypotheses and our pursuit of new science. That's how we've become better. Clyde, it is always delightful to catch up with you. It's been too long through COVID. Thank you so much for participating in this interview. And I look forward to seeing you in Chicago one of these days. And my friend, let me thank you for all you've done for the EP community over a few decades and all I've learned from you over that same time span. It's been a real pleasure. Thank you very much. Thank you, Clyde. Thank you.
Video Summary
In this segment of EP on EP, Eric Vrstovsky interviews Clyde Yancy, Chief of Cardiology at Northwestern Medicine. They discuss the intersectionality of arrhythmias and heart failure and the need for co-management. They highlight the similarities in risk factors for atrial fibrillation (AFib) and heart failure, emphasizing the importance of prevention strategies. They also discuss the need for more research and trials to understand the optimal management of patients with both conditions. They touch on topics such as tachyarrhythmia-mediated cardiomyopathy and the use of ICDs in heart failure patients. They acknowledge the challenges in determining who truly benefits from certain therapies and the need for better predictors. Overall, they emphasize the importance of ongoing research and collaboration between disciplines to improve patient outcomes.
Keywords
arrhythmias
heart failure
co-management
prevention strategies
patient outcomes
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