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EP on EP Episode 53 - Sudden Cardiac Arrest from E ...
EP on EP Episode 53
EP on EP Episode 53
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Hi, I'm Eric Prostowski, welcome to another segment of EP on EP. With me today is Dr. Jeremy Ruskin, long time friend and one of the leaders in our field of electrophysiology, who is currently the professor of medicine at Harvard University and also the founder and director emeritus of the cardiac arrhythmia service at MGH. Welcome Jeremy. Thanks Eric. It's nice to be here. So, you've done so much, but what I'd really like to talk about today is sudden cardiac death work. You published a seminal paper, back when, in the New England Journal on program STEM and sort of thinking of how to treat people who've had a cardiac arrest. Take us back there a little bit and tell us what your thinking was then, and then kind of from there, why we made transitions to a different way of approaching the problem. Well I think it's important to give you the history in terms of where things are when I started working in that field. So remember, back in the 70s, this was the work started in the late 70s. Sudden cardiac arrest was and still is a very common problem, but the management, the thinking was that these were all either MIs or acute ischemic events, and patients were, those who were lucky enough to get resuscitated, were admitted to the hospital. They typically had a cardiac cath with a coronary angiogram, and if they didn't have intervenable disease, they were, if they were lucky, put on a beta blocker and sent out, and that was it. That was the workup. And the assumption was that there was no sort of substrate problem here, that this was typically an ischemic problem, and that you treated the ischemia and let them go, and what we knew then was that the recurrence rate was about 35%, with a phenomenal mortality rate. So when we looked at these patients coming into the hospital, just looking at things as simple as an echo, it became obvious that a lot of these people had significant LV dysfunction, and they had not had an acute MI, and we, because it was the early days of program stimulation, wondered about whether or not these were, in some people, substrate abnormalities and whether or not inducible VTs may play a role in some of these people. And in fact, with program stimulation, about 60% of them had inducible rapid monomorphic VT. That was new. Right. You know, there had been one earlier study in out-of-hospital arrest using lower grades of stimulation that we used that said there was no inducibility, therefore this was not a substrate problem. And I remember... I don't know if you remember this. No, no, I remember... American Journal of Cardiology paper. Excuse me, American Journal of Medicine paper, what we used to call the Green Journal. The Green Journal. I don't remember that paper, but I grew up at Duke, so I was really an SVT guy at WPW, so when I then went to my first job at Indiana, suddenly I'm seeing all these... So your paper was critically important, because this was a different way of thinking of these patients. Totally different. Yeah. So I think what that paper did was, what that work did, was demonstrate that in at least a half of these people, if not more, there was a substrate abnormality. Right. And there were provocable arrhythmias that were reproducible. These were meaningful. They weren't nonspecific, because it was fast monomorphic VT. The other thing that we saw was that LV dysfunction was a very powerful predictor of recurrence. So we found that inducibility and suppression and LV dysfunction interacted in a very powerful way. So the EF was under 40, and you had an inducible arrhythmia, and you had a very high recurrence rate. What didn't pan out over the long term was the suppression with drugs during serial tests. Right. And I can tell you a whole bunch of papers I wrote that are sitting on a back shelf now, because who could care less, right? All of us were in that bed. That changed it. Did you cause me to do all that work? With the defibrillator. Well, I apologize. But I think the importance of that work was the demonstration that in a lot of these people, the problem was a fast monomorphic VT related to a substrate abnormality, and that the interaction of the electrical abnormality with EF were the two most powerful predictors. And in fact, inducibility is still an incredibly powerful predictor. That is true. Of event rate. So where do you think we are now? Now we're in the ICD era. Obviously, secondary prevention, I think everyone would agree. Where are we, in your opinion, on the primary prevention? I don't want to put you on the spot, but you know, there's two camps. Some people think we're putting in too many ICDs. Some people think we're not putting enough. Where do you think we are? Yeah, I don't mind you putting me on the spot at all. I've never been shy of expressing an opinion that may not be popular. Yeah, I think we put in too many. I mean, I think clearly the risk stratification schema that we have now is a blunt instrument, and I think it's a lot better than nothing. Which is the ejection fraction. It's basically EF. And I think that the value proposition, using EF alone, is not a good one. I think we put in far too many. Most of them, as you know, are never used. And for some reason or other, the impetus behind all the work on risk stratification is, at least from my perspective, seemingly ground to a halt. And I think that's very disappointing. I think we really have an obligation to resurrect all of that. I was just talking with someone this morning about T-web alternates, which is a very interesting predictor. That's gone nowhere. That has gone nowhere. And unfortunately, it was not used at all. So I think to answer your question directly, I fit firmly in the camp that would argue that we have a lot of work yet to do on finding risk stratification and improving the value proposition in terms of when we implant primary prevention. I'm with you a lot on that, with ischemic heart disease. But you know, I'm very impressed with the work being done with scar burdens in the non-ischemics, whether it be hypertrophic cardiomyopathy or the more common dilated. I'm starting to use that in my own risk stratification. If you have no scar, you're not at zero risk, but you're at pretty low risk. Don't you agree? I do. And I think it's very, very promising. I think that's exciting. But unfortunately, you can't kind of use that for the ischemics, right? So we're looking for a new tool. Yeah. I agree with you there. Well, Jeremy, it's been a wonderful discussion from where it started to where we are now. It's always wonderful having you. It's a pleasure. Thanks for having me. Thank you.
Video Summary
In this video segment, Dr. Jeremy Ruskin discusses his work on sudden cardiac death and the changes in the approach to treating cardiac arrest patients. In the past, the focus was on treating ischemia, assuming it was the main cause, but Dr. Ruskin's research showed that many patients had substrate abnormalities and inducible VTs. He also found that LV dysfunction was a predictor of recurrence. The use of drugs for suppression during serial tests did not have long-term success. Now, in the era of ICDs, there is a debate on the appropriate use of primary prevention. Dr. Ruskin believes that there is still work to be done in risk stratification and finding better tools.
Keywords
sudden cardiac death
changes in approach
treating cardiac arrest
LV dysfunction
ICDs
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