Episode 59 — Takotsubo Cardiomyopathy With Vincent Sorrell
Highlights
- The Different Patterns of Postmenopausal Women Presenting with Stress Cardiomyopathy
Key takeaways:
- Stress cardiomyopathy can present with a variety of different patterns,.
- Recurrence rates are high, with up to 30% of patients returning within the first four years after their first episode.
Transcript:
Speaker 1
So we really don't know. We can just categorize the majority of postmenopausal women worldwide and certainly in the US. They present what stress cardiomyopathy that involves the apex and the apex actually balloons out. That's pretty typical. But we do know that 10% or more, certainly some of the patients you described initially in your presentation that you see in the neuro ICU that have an insult inside their cranium, they actually present sometimes more commonly with the atypical pattern, meaning the apex is spared, but the mid-ventricle is actually dysfunctional or some other component, some other region of the heart is atypical. Let me also point out that, you know, we'll talk about this, I'm sure, but recurrence rate is a real thing. We know that patients who have Takasubo or stress cardiomyopathy once can come back again at another date. What we're starting to learn because we're studying this more is that they may present with a different pattern when they come back. So they come into us with the classic atypical ballooning and then they come back with regional abnormalities. And we take off the table saying, oh, it doesn't look like the last one. It's probably ACS this time. And it turns out it's actually another variant form of stress cardiomyopathy. So it's pretty fascinating disease.
Speaker 3
Is recurrence common? That's not something I've ever considered. Absolutely.
Speaker 1
Unfortunately, we are starting to understand that recurrence is a real thing. Recurrence rates can occur up to 30% in the first four years after the first event. (Time 0:08:04)
- Taka Subo: A New Diagnosis of Exclusion for Acute Coronary Syndrome
Key takeaways:
- Recurrence rates can occur up to 30% in the first four years after the first event.
- Beta blockers may increase the risk of recurrence.
- Noninvasive measures can help guide the diagnosis of ACS.
Transcript:
Speaker 1
Unfortunately, we are starting to understand that recurrence is a real thing. Recurrence rates can occur up to 30% in the first four years after the first event. And we're starting to try to figure out whether the beta blockers that people have employed for treating stress cardiomyopathy and then they withdraw them at a certain point, whether that withdrawal actually increases the risk or not. So many of the guidelines now are saying, let's not use beta blockers. Let's focus on ACE and ARB treatment. I know we'll talk more about treatment, but they're starting to guide us away from beta blocker therapy because of that.
Speaker 2
Interesting. Okay. So you can't eliminate ACS then. It sounds like from this based on the echo alone. And you mentioned a couple of other things like myocarditis. So where do you go from here? Is Taka Subo something that you can put your finger on or is it more of a diagnosis of exclusion?
Speaker 1
So general thinking is it's a diagnosis of exclusion that you have to know the coronaries and if the coronaries are okay, then you say, aha, it's what I thought it was before I looked at the coronaries and stress cardiomyopathy. I'm working really hard on trying to come up with noninvasive measures. We know that there's a few things that can guide us and I could walk through those briefly. The ECG pattern is helpful. ST elevation can occur in either T-wave inversion, can occur in either nonspecific ST segment changes, can occur in either. ST elevation in lead V1 or limb lead one is pretty unusual in Taka Subo. So if you see that, start thinking more ACS. (Time 0:09:20)
- Noninvasive Measures to Guide Diagnosis of Acute Coronary Syndrome
Key takeaways:
- The diagnosis of ACS is based on the presence of troponin elevations and other biomarkers,.
- The degree of troponin elevation correlates well with the ejection fraction.
Transcript:
Speaker 1
So general thinking is it's a diagnosis of exclusion that you have to know the coronaries and if the coronaries are okay, then you say, aha, it's what I thought it was before I looked at the coronaries and stress cardiomyopathy. I'm working really hard on trying to come up with noninvasive measures. We know that there's a few things that can guide us and I could walk through those briefly. The ECG pattern is helpful. ST elevation can occur in either T-wave inversion, can occur in either nonspecific ST segment changes, can occur in either. ST elevation in lead V1 or limb lead one is pretty unusual in Taka Subo. So if you see that, start thinking more ACS. The degree of the troponin elevation is higher in ACS than it is in stress cardiomyopathy. And the correlation to the elevation of the biomarkers, the troponin, fits pretty nicely to the ejection fraction. So you can sort of take a look and make sure that it matches well because it will in stress cardiomyopathy. Okay.
Speaker 2
So do you see (Time 0:10:15)
- Alternative Therapies for Cardiac Arrest
Key takeaways:
- There is a lack of good data on calcium sensitizers and levo, and there are no known alternative treatments.
- In the acute phase, beta blockade is not typically entertained.
- The current mantra is to go with what works in the site.
Transcript:
Speaker 1
So you're right. So there is this idea of calcium sensitizers and levo, whatever that medicine is that people have kind of studied, but there's very poor data on it. I think there's some alternative options. They're not really worked out through randomized controlled trials. We just don't have enough experience. And what we do know, right, is in the short term, these patients can be, you know, cardiogenic shock and deadly. And we treat them to get them through that initial transient event that they had. The trigger has already occurred. I'm not sure that we believe we're adding more triggers, although it's definitely something that's in the back of our minds, right? And I know, you know, there's a patient I recall that had ventricular tachycardia. And we were asked to see and they had an apical ballooning syndrome. And everybody was like, oh, they had VT as an event from their apical ballooning syndrome. And as we pieced it together, she actually had it sounds like a VT event. And in part of her code got epi and we had an echo before and after. So she got the event after the treatment for her VT. So these things can happen. You're right. But I think because of the lack of randomized trials and alternative therapies, we have to go with what we know works in the site.
Speaker 3
And it sounds like that would also mean in the acute phase, you wouldn't be entertaining things like beta blockade.
Speaker 1
That's correct. And if anything, we're starting to go away from that. I think that's the current mantra out there, but we have a lot more work to do. (Time 0:21:52)
- Managing Cardiomyopathy in the Acute Setting
Key takeaways:
- In cases of progressive stress cardiomyopathy, the patient will typically recover within a few weeks, and almost all recover within three months.
- If the cardiomyopathy is due to stress, it will run its course and the patient will turn.
Transcript:
Speaker 1
So at that point, we'll go through the usual algorithm that may actually lead to mechanical circulatory support of whatever we need. So these patients can crash and burn and die in that acute setting if they're presenting with a progressive stress cardiomyopathy. So whether it's due to the norepi, whether it's due to the natural course, I'm not sure that I could say that, but if it is progressing, then we also have to accelerate our care and offer all the tools that we have at our disposal. Okay.
Speaker 2
So basically right now, we just treat this woman like sort of garden variety, septic plus cardiogenic shock.
Speaker 1
I think so. And again, if this is due to stress cardiomyopathy, it will run its course and she should turn. Okay.
Speaker 2
So we're doing all that. Things appear to be getting better. She's on antibiotics. She's getting all the standard sepsis treatment. What do we do? At what point are you looking at starting to, quote, manage the cardiomyopathy? Yeah.
Speaker 1
So the natural history of stress cardiomyopathy is that 95 plus percent go through this recovery period. Basically it happens at a variable rate, but within a couple of weeks, most people will have recovered, almost all recover within three months. (Time 0:24:07)
- Differentiating Stress Cardiomyopathy from Sepsis Cardiomyopathy
Key takeaways:
- Sepsis cardiomyopathy is a condition that is caused by the inflammation of the heart caused by sepsis.
- Sepsis cardiomyopathy is a condition that is characterized by an increase in the amount of myocardium that is regionally dysfunctional.
- The likelihood of a good outcome for a sepsis cardiomyopathy patient depends on the severity of their condition and the presence or absence of coronary calcium.
Transcript:
Speaker 1
So you're right. I mean, septic cardiomyopathy or a sepsis cardiomyopathy or we could just say an ICU cardiomyopathy because that's a lot of what we see. We looked at it here. We pulled it at UK. We went ahead and pulled all of our patients who had presented with sepsis. We looked at their biomarkers. We looked at also two other things, what their echo was and what their chest CT was. And on the chest CT, we looked for coronary calcium. And so we were able to categorize the likelihood of discharge from the ICU, healthy or not healthy based on an EF above or under 50 and the chest CT, which is free because it's already there. People just don't look at it. But the chest CT looking at the coronaries, coronary calcium versus no calcium. And if you had both of those, your chances of having a good cardiac outcome or a good ICU outcome were really bad. So an EF less than 50 and a positive calcium on your chest CT was actually a bad marker. But if you didn't have either of those, you were actually going to do really well and fly through the ICU. Coming back to your point about, is it different? I think it's an overlap, but it is definitely different. The idea that you could subtly create a huge amount of myocardium regionally dysfunctional with the likelihood that it's all going to recover no matter what we do is absolutely fascinating and unique to stress cardiomyopathy. That's very different than that chronic stressor of the ICU or the sepsis or those other things, which is almost always global.
Speaker 3
So the picture you'd expect in the septic patient might be a little less sudden, maybe less rapid to (Time 0:43:04)