Episode 59: Takotsubo cardiomyopathy with Vincent Sorrell

Hey everyone, I'm Brandon Odo. And I'm Brian Bulling. And this is Critical Care Scenarios, the podcast where we use clinical cases, narrative storytelling, and expert guests to impact how critical care is practiced in the real world. All right everyone, welcome back to Critical Care Scenarios. We have a, I think, a really interesting topic for you today. We are sitting down with Dr. Vincent Sorrel, who's a cardiologist over at the University of Kentucky, which is Brian's neck of the woods. He helped develop their advanced cardiovascular imaging program. He's the acting chief at the Division of Cardiovascular Medicine and the acting director of the Gilheart and vascular Institute there. But he's done a lot of focused research on the topic of stress or Takasubo cardiomyopathy. And we thought it was really something worth diving into. This is certainly not something that is the zebra I think we all once believed it was. We come across it not infrequently. But I'm not sure how deep our understanding of it is, at least in the ICU. So Brian's going to bring us through a little bit of a case to help us work around this topic and see what we can learn. All right, so before we get started, I just want to, I want to say something real quick and talk a little bit about this disease. So I think most of us probably learned of this as Broken Heart Syndrome as more of a, you know, the grieving widow shows up with chest pain and it's all from psychological stress. But I've seen in seven years in the ICU, mostly in the neuro ICU, but also some of this surgical ICU. I've seen a lot of cases of this that don't have anything to do with psychological stress. And so I think we'd like to get a little deeper into like Brian said, this isn't not the zebra that we thought it used to think it was. And so I want to talk a little bit about maybe the kind of Takasubo or stress cardiomyopathy that we're less familiar with that that's brought on by physiological stress of critical illness. So Dr. Surrell, you are working as usual in cardiology consults and you get a call from the emergency department. They have a patient they'd like you to see. So this is a lady, she's a 65 year old who came in originally presenting with about a one week history of cough, fever, chills, slightly tachycardic. And you're wondering, why are you calling cardiology? Well, during the course of their workup, they got an EKG because of course they did. And the EKG showed diffuse sort of global ST elevation in all the leads. Now she's not complaining of chest pain, but they went ahead and sent some Trimpronens because of course they did. And they're really concerned because this is an older lady who's unwell appearing and you know older women sometimes present atypically with MI symptoms. And they're really worried about missing an MI. So they called you and said, will you come and look at this lady? So what are your first thoughts as you head down to the ED to see this woman? Thanks for having me. I look forward to talking through these cases and exploring a little bit of Broken Heart syndrome which as you rightly described is something that we're fascinated by in the world of cardiology, that it masks its presentation, that it comes at us from different angles and that most of us are like, oh, I wasn't thinking that's what it was and it turned out that's what it was. So it usually catches a soft guard and it shouldn't. So I would say coming back to your case, the first thing that struck me was you said 65 years old and you said older woman. Those two things we got to get out of the nomenclature. I'm getting way too close to that age to be considering that to be older. But post-menopausal, we'll say that. Yeah, there you go. And so what's my thoughts, right? She has a fever, she has a cough, she's in the ICU. So obviously you guys are chasing her for what's going on in her lung fields, whether she's got pneumonia, some sort of sepsis, et cetera. The diffuse ST elevation, the tropes is certainly something that worries us. And it includes that caveat of pericarditis, malcarditis, also acute coronary syndrome. And you should never ever today, I believe, think of a post-menopausal woman with acute coronary syndrome and not also say, or could it be a stress cardiopathy. So I think this differential that we immediately have can be somewhat further stratified with a quick echo. And that's where I'd be looking at her care. Okay, so you're going to do an echo. And what are you sort of expecting to find? Yeah, and you know, again, I go into it obviously with equal pose. I can find an absolutely normal-sized heart contracting normally, and I can find everything else. I can find a dilated heart that we weren't expecting because she has profound inflammatory malcarditis. I could find the regional pattern of apical ballooning that we see as the most classical form of a stress cardiomyopathy. I could see a blown-out inferior lateral wall with a very regional pattern that makes us think coronary disease. So there's a whole host of things that are immediately discriminatory on a well-performed echo. If you go into it with the right vision and you're asking yourself the right questions, right? Echo is only as good as what those questions are and you know how to interpret it. Yeah, okay. So for the purposes of this, I'm going to make our ED colleagues look a little bad. We know that they're actually pretty good at echo and they know their stuff. But it helps to have someone who needs stuff explained to them, right? So you get down there and the ED resident says, oh, I did an echo. I did a bedside echo. It was really weird because I expected to see regional wall motion abnormality, and it kind of did, but it didn't fit the typical kind of ACS pattern, but it didn't fit the apical ballooning pattern either. It's got sort of decent contraction at the apex, but really poor mid-ventricular contraction. And then okay contraction at the base of the ventricle, but it doesn't fit any coronary artery distribution. And so I'm really confused. What do you make of that? Yeah, it's a really nice description, first of all, and you described a regional pattern in a non-coronary territory. So as a cardiologist, I'm fully aware that coronary territories are generalized, but not uniquely specific to the patient. So patients can have regional patterns. Turns out they are coronary in those individuals, even though they don't fit our roadmap for what is anticipated for a coronary distribution. So I don't completely eliminate ACS from that story, but I'm absolutely raising the bar on these atypical presentations of a stress cardiomyopathy, which could be mid-ventricular, basal, or anything else. The other differential to get beyond ACS and Takasubo or ACS and stress cardiomyopathy to be more specific includes some other oddball things, like cardiac sarcoid, infiltrations, coronary cardiac cancers, and weird things like that that can affect regionally, but my differential is pretty wide. Okay, so I think most of us learned apical ballooning syndrome as sort of another term for this Takasubo stress cardiomyopathy, but it's true, right? It doesn't have to be the apex that balloons out, right? It could be dysfunction in other areas of the ventricle. Absolutely, and that's why we probably shouldn't use the term Takasubo as much. We should say stress cardiomyopathy, aka typical or non-typical, if it's typical, then it fits Takasubo. Okay. So I guess let's talk about that real quick. What is typical Takasubo versus atypical, and who are you most likely to see each in? Yeah, so we really don't know. We can just categorize the majority of postmenopausal women worldwide and certainly in the US. They present with 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 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. They come into us with the classic apical ballooning and then they come back with regional abnormalities and we take off the table saying, oh, it doesn't look like their last one, it's probably ACS this time, and it turns out it's actually another variant form of stress cardiomyopathy. It's pretty fascinating disease. Is recurrence common? That's not something I've ever considered. Absolutely. 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. 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. Many of the guidelines now are saying, let's not use beta blockers, let's focus on ACE and ARB treatment. We'll talk more about treatment, but they're starting to guide us away from beta blocker therapy because of that. Interesting. You can't eliminate ACS then, it sounds like, from this based on the ECHO alone. You mentioned a couple of other things like myocarditis. 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? 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 it's stress cardiomyopathy. I'm working really hard on trying to come up with non-invasive 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, non-specific ST segment changes can occur in either. ST elevation in lead V1 or limb lead I is pretty unusual in Taka Subo. If you see that, start thinking more ACS. The degree of the troponin elevation is higher in ACS than it is in stress cardiomyopathy. The correlation to the elevation of the biomarkers, the troponin, fits pretty nicely to the ejection fraction. You can take a look and make sure that it matches well because it will in stress cardiomyopathy. Do you see the same delta rise interoponins with stress cardiomyopathy that we see in ACS or is it more, it goes up and stays up? Similar to acute malcardioin function, the reason it goes up and comes down is because we intervened. If you missed the fact that ACS was an occluded coronary and you didn't intervene, it will go up and stay up. I think you'll see the same thing with stress cardiomyopathy. It will go up and it will fall. That's what we should see in our ACS because we're intervening. Peyton arteries wash out pretty good. Sure. We check the troponin at zero hour and two hour to see if there's a delta rise to differentiate ACS from some other troponin leakage. Do you see that same sort of rise initially with stress cardiomyopathy? Yes, to a less degree though, again, the full extent is not quite as high. I think again, we have different criteria. I think there's the intertact, if you will, measurement where it's a clinical estimate. It's a diagnostic score, if you will, to help us figure out if we think it's stress cardiomyopathy or ACS. It's imperfect. In a patient who's sick, we're not going to be waiting around doing scores. We're going to assume it's ACS until we prove otherwise. In a patient who's stable, it's another tool that you can use, which really looks at patients, gender, patient sex, underlying triggers, the event that occurred that made them present. Those are all things that can be used. My problem with the intertact score is that a very high score, very low score helpful, but unfortunately the ones in the middle, which most of our patients are not very helpful and we need more information. The patient who's doing well, what I'm trying to do with non-invasive imaging using echocriteria is to say, okay, this patient, we can save and do a non-invasive cardiac CTA, get a non-invasive coronary, and if it's normal, we can stop. We can save it in the evasive angiogram. In other patients where we don't have certain features or there's certain bigger concerns like I described on the ECG or the height of the troponin, they need to go to the cathode. Do you encounter situations where there's both? I mean, you think there's maybe some element of a stress card mouthy, but maybe you cat them and there is disease and you're not really sure if there's both contributing or one provoked the other or what? Yeah, so I do live in a pretty good school where I'm able to separate that out a little bit. I don't believe the coronaries have to be quote normal. I believe they have to not fit a plaque rupture in the wall motion territory. So I think the original guidelines were written normal coronaries. That was a mistake. It should have said, you know, living in society today, a 65-year-old woman in Kentucky, she's got coronary disease. Does it explain what we see and the answer to that is no, then it's stress cardiomyopathy? Or in our setting, a lot of what we're seeing is not necessarily plaque ruptures, but more of demand related ischemias. And then I don't know how to piece those apart because it's not really an acute event either. Yeah, so again, at the end of the scheme, you really shouldn't give us that. You know, in acute malcardo injury, right, you can get a bump in a fall, but it's usually not very much. You shouldn't get the dramatic, transient EKG changes. You usually don't have the clinical presentation that's more cloudy, right, the sudden event. But it happens. I get it. You guys certainly see sick patients with reduced function elevated tropes in wall motion abnormalities. A lot of that. All right, so with this patient now, what's your next step in the workup? So what did I see on the echo? The echo is pretty much as described by the resident you see, reduced EF, say around 40%, 30% to 40%. You know, some regional wall motion abnormality, but not the typical coronary distribution pattern. Decent contraction at the apex, almost a kinetic in the mid-ventricle and hypokinetic at the base. Okay, so reduced function, regional dysfunction, abnormal EKG, and how high were her biomarkers? How high was her tropon? Oh gosh, let's say, you know... Just say ACS high or stress-critical apathy high? Yeah, not quite ACS high. We'll say that. Okay. So then the final question is clinically, right? Does she need to go to an ICU? Does she need to go to a floor? Where were we fitting? What does she look like? So she's hypotensive, so far responsive to fluids, but getting worse, like not looking great. Her pulmonary status is not great, and the ED is concerned that she's going to need some BiPAP or possibly even intubation pretty soon. So she's definitely going to end up in the ICU. Yeah, so we need our course. I mean, we need to make sure that that's off the table. The question is, do you need to go now or do you need to go at a different time? And that's a decision you make really by looking at her, by seeing her and seeing if there's ST elevation or not on the ECG. If there's any ST elevation at all, you've probably got to look at the coronaries. Because the one thing we can't do here, we can't take the chance that we have a time bomb going with mild cardio non-recovery in that window of time. And if we pass up that window, we pass up the recovery of function. We can't let that happen. And so that's what I'm always trying to decide is clinically, do I believe, that I could identify something that is killing muscle, that if I don't intervene now, the muscle will die. If that's a possibility, you've got to go to the cath lab. Okay. So she's got ST elevation on her EKG, but it's sort of global, like I said, it almost fits a paracarditis kind of picture, right, where you get it everywhere. Not really the stimmy type of picture, but would you still want to take her to the cath lab? Again, I mean, it's hard to say on a podcast as opposed to seeing the patient, but I do think that my sentiment doesn't change. Okay. So even if I'm capping her with the thought that it won't be obstructed, it won't be occluded and I won't have to intervene, I can't take the risk of missing that. Okay. What I often do in those cases is I'll swing through a cardiac CT on the way to the ICU, and I may have normal cores, and that could explain everything. And that's kind of a judgment call that I make on the fly. Some of the clinical scenarios, I guess, for the people listening to think about when you might want to do CTA is what if this lady has a big lung cancer and she's got a terminal malignancy? What if she's got a brain bleed and it prevents us from doing a lot of anticoagulation? What if she's older, let's say not 65, but 95, or she's got to bought a frailty or bleeding diethhesis? I think in those settings, you could make that leap of faith that let's go noninvasively and maybe get all the information we need and accept that small chance that I'm going to diagnose and acute am I in the CT suite, which I hate to do, but on occasion I will. Okay. Let's say some of our listeners are at a smaller hospital, they don't have a lot of advanced stuff. What are you talking about when you say cardiac CT? Yeah, so noninvasive coronary angiogram. Okay, so just like a CTA? A CTA. Okay. All right, so let's say we do that and you find you don't see any evidence of acute obstruction. So we're going up to the ICU. She's coming along, looking septic, looking kind of worse. The ICU team feels like, hey, we probably need to intubate this lady. Is there anything we need to be aware of with her heart function before we intubate her? So that's where I'd want to be looking at the echo myself, listening to see if there's a murmur, looking at the echo. And these patients, I always want to categorize into two groups. Right away, she's stable or unstable, she's unstable. And then the second most important and equally important is outflow obstruction or no outflow obstruction because your management is going to diverge greatly based on the presence or absence of outflow obstruction. And with stress cardiopathy, we see this not uncommonly, probably more common than we actually diagnose it because we sometimes find ourselves going down the pathway of conventional treatment that's not working. And then again, we back into a diagnosis because we weren't considering it upfront. Okay. So we'll just assume for the purposes of this. We don't see anything that would preclude sort of a normal RSI intubation. So we intubate her, but now she's becoming more and more hypotensive. They are talking about starting some norepinephrine because we feel like she's septic. But if this is cardiogenic shock, that may not be the best. So what advice can you give us on that? Yeah. This is where I call in my ICU colleagues to help guide her care and offer their insights as well. I think, you know, again, if there's no obstruction, then you're going to have to treat the shock the way that you would normally treat shock and not worry about it. So no air epi is fine. It's the way to go. If she has an obstruction, then of course, the concern that I have is increasing her outflow gradient and worsening her stroke volume in exact opposite pattern to what we were hoping we were going to get with the isotropic therapy. And of course, volumes are going to go in the opposite way as well. Right. If it turns out that she gets into serious hard failure, more pulmonary demon, we think we have to afterload her. If she's got outflow obstruction, all the things we're going to do for afterload are the exact opposite things we should be doing where we probably should be giving fluid to increase her LV size would actually be diureasing and afterloading and thinking balloon pumps, which would be the opposite of what we should do. So again, a lot comes down to what's happening at her outflow, how big is her heart and how big is that basal contraction versus not? If she has an offload obstruction, then yeah, nor it'd be fine. So it sounds like you're saying that if there's no outflow tract obstruction, you can pretty much treat this patient human dynamically like anyone else, which is interesting because I think a lot of people's understanding of this disease is that it's somehow catacolamine mediated and using kind of adenergic agents may in some intrinsic way worsen it. But it sounds like not so much, huh? So you're right. So there is this idea of right 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 that 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. And it sounds like that would also mean in the acute phase, you wouldn't be entertaining things like beta blockade. 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. If we get into a point where we've started norepinephrine and that's actually making her cardiogenic component of her shock worse, would you then advocate switching to epinephrine or just adding something to give you some inotropic support on top of the norepinephrine or what's the way to go there? Yeah. When you say it's worsening, what do you actually mean? So let's say despite the norepinephrine, she continues to be hypertensive. We re-echo her EF appears to be worse. It looks more like a cardiogenic shock picture, but of course probably combined with some septic shock. So we have a mixed picture. Yeah. 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. So basically right now, we just treat this woman like sort of garden variety septic plus cardiogenic shock. I think so. And again, if this is due to stress cardiomyopathy, it will run its course and she should turn. Okay. 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. So the natural history of stress cardiomyopathy is that 95 plus percent go through this recovery period. Usually it happens at a variable rate, but within a couple of weeks, most people will have recovered, almost all recover within three months. That first few days, two weeks is variable, highly variable. You'll see some people that just have this dramatic recovery. I'd be fascinated to know the genetics behind why some recover on the rapid curve and why some are much slower. Maybe it is what Brandon was questioning is our therapies are leading to that. We need to understand that better. We just don't know. But in theory, she'll turn this quarter pretty quickly. And then we have to start saying, okay, what can we do to try to prevent a second recurrence? What can we do to help her recover? The good news is you do nothing. It should recover. The average news is that we have some guidelines to drive us that ACEs and ARBs are probably the current recommended therapy. There's debate there as well. From my heart failure experts, we give those therapies when there's reduced function for benefit on this neural hormonal axis. Well the neural hormonal axis actually works on months. Her value of that therapy in three months makes no sense because she should have recovered by then. So there must be more to the story that we really don't know. But right now, based on just really expert opinion, we recommend ACEs ARBs to get to that next echo to show that it's completely recovered before you even talk of stopping them. We usually then continue them for at least six months before we make that withdrawal. And beta blockers are a little controversial right now. So you come back in the next day and she's looking more stable. She still has very poor EF and her blood pressure is better. She's on a low dose of norepinephrine, a low dose of epinephrine together. But she's much more hemodynamic stable than she was before. And you've a med student is with you who says Dr. Shiloh I was reading up on this last night and it seems that one of the big complications of this is thromboembolism formation in the LV. Do we need to be concerned about that? Do we need to be concerned about putting her on some sort of anticoagulation? And also I read a little bit but I didn't read a lot. So why do we need to worry about this? So first of all, I love the medical student. Well done. I think they were hit it on the head that as soon as you can start any coagulation for large wall motion abnormalities regardless of the underlying etiology, we probably should be doing that. I think we probably don't pull the trigger as much as we should. If we look at the echolitature, it's pretty robust that patients with large wall motion abnormalities followed serially develop clots. And that number is somewhere between what? Five to 30 percent. It's not a small number. Now not all of those clots, imbalize. So yes, we see them on echo but clinically they don't have strokes. So we believe in our practice that it happens less commonly than it really does. So I think we should pull the trigger sooner than later. Start any coagulation. So in the hospital, a little more likely to wait any coagulation, get them home or any coagulation, close follow up and then when their heart recovers, you can stop it. Is that regardless of the anatomic distribution? I think the apex is worse. The apex is worse for a few reasons. Right? I'm an imaging guy. So for me, right, when I watch the blood flow come in, I could tell you exactly the vector flow of how it hits the interlateral wall rotates around the apex and then comes out the outflow track. There's a beautiful sort of architecture to the flow patterns. As your LV apex stops doing what it's supposed to do, guess what the flow does? It starts becoming more chaotic, stops doing what it should do, understanding our normal makeup for what creates thrombus. You start interrupting flow, you're going to end up getting a clot. So the apex is unique in its ability to form clots. So are you going to put her on some sort of therapeutic anacolulation like you would for ACS like a heparin drip or something? Yeah, I think IV or a low molecular weight, sub-Q heparin during her initial course is absolutely appropriate and then oral anacolulation, a discharge, continuing for at least three months I say for stroke prophylaxis. Okay. Do you have a drug of choice for that or? No. Whatever Walmart gets you for $5. So no preference between warfarin versus Revroxaban versus a Pixaban? Not for me. I'm old school and I think warfarin is awful and so I do everything I can to avoid it. Okay, fair enough. All right. Okay. So she's getting better. She's extubated now. He would do a stable off pressers ready to transfer out of the ICU. Does she need to go to the cardiology service or does she need to go to a medicine service? Yeah, that's a great question and I don't know that we have the answers again. I think if she comes to cardiology service, I'll tell you some of the things that I would strive for and I would hope if she went somewhere else they would do as well. Number one, really careful risk assessment, right? Does she have another reason for an aspirin statin and the underlying coronary disease risk factors? I want to make sure we're on top of those. Two, we still haven't seen her coronaries. We probably would want to do that at some point in her future. Three, I'd be getting a really good history on her depression, anxiety, psych history. Does she need treatment there? We can't ignore the fact that that's a common denominator in our postmenopausal women who have these events and therefore maybe we could lower a recurrence rate by treating some of these other factors. Hormone replacement, it's a controversial topic but it should be discussed with her and an individual base is probably treated. And then lastly, cardiac rehab, she does have dysfunction and getting her into rehab, we believe will lower her event rates and increase her survival. People who are used to treating heart failure from other causes, it sounds like this is long-term meaning over weeks to months going to be similar but different. She doesn't need things specific to ACS like aspirin and statins and things. The human dynamics of heart failure are the same so if she needs a diuresis or after blood reduction she still needs that. Beta blockers plus minus it sounds like in an anequagulation again kind of as needed. So the big difference is maybe clean coronaries and the timeline hopefully is not long. So we're not trying to do prevention over a period of years. Hopefully this is all going to be better in a few months but they still have to be treated in the meantime. Absolutely. And again, the beta blocker I think I used to be gun hosts. Absolutely. I think the literature today tells me no. So I'm actually not doing beta blockers today in these patients. I know a lot of my colleagues will talk as well about the role of a possible, you know, jacket ICD, right? What are they called? I never recommend them to anybody. Life Fest. Thank you. That's the word. So I'm not a fan. I think that that is really poor on that but I know people if they had had, you know, ventricated arrhythmia during her presentation, realizing that this is a short-term event with a relative risk, they might recommend that on a one-to-one basis. So these people may have risk of sudden death but maybe not as much as someone with reduced DF of other causes. Yeah. So again, putting it into terms, if you look at control groups, control groups of stress cardiomyopathy compared to people without coronary disease, they do worse. Compared to people with coronary disease, they do better. So they're somewhere in between. And you would move to the beta blocker if they did have obstruction that you saw on their echoes? Abstruction in the outflow track, I mean? Yeah. Or yeah, not coronary obstruction. No, no, yeah. Okay. Yeah. So yes, I think in that setting, right, as part of your initial treatment with the hyper-dynamic base, they may need a beta blocker to help that treatment. Usually it's, you know, withdrawing the inotrope and increasing fluid. You don't need to go the beta blocker route but occasionally you may. So if that had resolved by the time they're leaving the hospital, they don't need to stay on it. Correct. She's better and ready for discharge. We've kind of touched on some of those things. You know, this is sort of outside the critical care wheelhouse anyway. So I do want to talk a little bit though. We see, so this lady, she happens to show up in the ED and gets a, you know, quote, cardiac workup and that's how this is discovered. We see these a lot in the neuro ICU kind of incidentally, right? We get somebody with a great example of a high grade subarachnoid hemorrhage who is hemodynamically unstable and only mildly responsive to sort of the standard, you know, norepinephrine vasopressin. We do a bedside echo and see, holy cow, look at this EF. It's really crappy. And it doesn't seem to fit the normal ACS pattern. It looks kind of like stress cardiomyopathy. At what point does the average ICU team need to get cardiology involved with these patients? Is this something that cardiology needs to be following or is this something that can largely be managed by people who understand how to manage heart failure, sort of garden variety, heart failure and shock? Yeah. So again, I don't have a specific black and white answer for you, but I think on an individual basis, there will definitely be patients that are not responding to your initial treatment plan. I think when that happens, you call us on board. You know, don't let yourself go too far down the pathway of, well, I tried this and it works. I'll try that. Well, it didn't work. So I'll try this. As you get farther away from the things that you're comfortable with that should reply that, right, they should respond to that it's probably time to get us involved. We do have some extra tools, right? When we start talking about mechanical circulatory support, the problem with cardiogenic shock today and the death rates that are associated with it are in part due to the fact we make our decisions too late, right? So we're starting to understand this time to device is a really important timeline. And so getting us involved as early as never going to be a problem, we can always assist and help. Getting us involved late can be a problem because the tools that can be offered may be off the table by then. Okay. And so you're, when you said mechanical circulatory support, I assume we're talking about probably starting off with things like balloon pump. Yeah, balloon pump ECMO all the way down to LVAD, whatever we have to do. We know that, you know, young people get full boat, whatever choices we have at our disposal. Okay. And so if you're at a center, let's say you're at a smaller community hospital, and this looks like cardiogenic shock and your cardiologist there feels comfortable managing cardiogenic shock, but they don't really do anything beyond the occasional balloon pump. At what point do they need to be starting to think about calling somebody like you at a big academic center that has ECMO, that has VADs, that has impelas and stuff like that? So the ECMO is probably helpful as well, right? A patient whose heart fits the description of what our patient had in this scenario probably wouldn't need that transfer to a bigger center because you kind of anticipate the course would follow like the course you described. But let's say that that heart was actually six and a half centimeters and the EF was under 20% and the stroke volume, if they knew, you know, if they were calculating that not invasively was markedly reduced, then now you've got a patient who likely, predictably, is not going to respond to the therapies they have at their disposal. And depending on how young they are or how old they are, it could happen very fast, right? Young people, it may just be delayed because they have incredible ability to compensate. So once they do hit that curve, it's too late to transfer them. Whereas older people may already start to look like, gosh, I wish I transferred them, but you know, it's happening pretty fast. Is there a way to predict that sort of thing other than just being a good cardiologist and knowing what an echo should look like or? So there's value in the EF. You know, we published a paper on what the EF is going on, which if you take a look at that, it actually pronounces what the EF is going on. It's a wonderful paper, but it actually walks through this. And I think in this scenario, there's value in the EF, right? I mean, if the EF is 40 versus EF at 20, it sends important messaging. We don't have great tools. I think an EF with a dilated heart is different than an EF with a smaller heart. Sometimes we don't think that way, but clinically the way these patients present it has different meanings. Well, I think that from my end, pretty much covers it. Brandon, do you have anything else you want to add? I guess I have a few just little questions. What's the deal with the RV? There's a common to see RV involvement in this kind of distribution. Is that atypical, but it can happen? So great question. The RV does get involved. I don't recall exactly what the percent is. I would say it's probably in that order of 10 to 30% of the time. I love it when the RV is involved, to be honest with you, because when I'm looking at a regional wall motion abnormality that knocked out a portion of the RV, it almost guarantees that this isn't due to an underlying coronary pattern because the RV is perfused by the RCA. The RCA is what gives off the right coronary artery is what gives off the RV marginal branches. That means the basal inferior in-ferosceptal wall is going to be involved if you get a regional RV dysfunction. The combination of an LV apex involving an RV tells me that those coronaries don't make sense. It has to be stress cardiomyopathy. I actually like it when it happens. That's more diagnostic than just the LV. Yeah, absolutely. The RV goes down in, as you know, inferior in-farks, they're the ones that drive you crazy because they have the RV involvement. So I guess also on the diagnostic side, we talked about, you know, an ordinary in ACS, your troponin should fall only if you intervene, or I guess if you waited long enough that they absolutely completed their in-farked. Whereas in Takasubo, really, it should start to resolve. So if you had not intervened on someone, you're like, this really looks like stress cardiomyopathy, but you trend their troponins and it continues to go up. Does that suggest you might have missed ACS or I guess other way around? You're like, this could be ACS, but by the time you get around to it, the tropes are coming down already. Does that make you feel better? Yeah. So, you know, again, I think I'm trying to put this into my clinical right acumen here. I don't ever want to be in a situation where the serial nature of the troponin helps me make a diagnosis. Oh gosh, it was ACS. I wish I had done something different, right? So yeah, so for me, you know, that the reason we do the two in four hours and I pushed hard for that delta concept here was because of that time window, right? We do not want myocardium that's in jeopardy to stay in jeopardy any longer than it has to. And so getting those coronaries, getting that coronary flow to resolve is critically important. But your concept is right. I think the way you described it is correct. We have more than once in my life, unfortunately, right? I've seen patients where it just stayed up and I was scratching my head the next day, 24 hours later and I'm like, damn. And sure enough, I take a look, I get a CTA, I get a coronary angiogram and they've got a totally occluded vessel that just didn't fit the classic presentation. That has happened. Sometimes I make that diagnosis with MRI. We do so many cardiac MRIs that there's a certain pattern on MRI where I get patients sent to me, sometimes really young patients for possible malcarditis. And I call them back and say, hey, thanks for sending me this study. It's a beautiful example of a completed infarct. And they're 18, 19 years old. You're like, what happened? Well, while we're talking about troponins, so I know troponins are sort of, we kind of love to hate them in the ICU because they're almost always elevated, right? Yeah, almost every time I draw a troponin on a patient, and I see it's elevated. So is it even worth getting them and when? Like when is it really valuable to get troponins? Like this lady comes in the ED, I would say, sure, yeah, right? She's in the ED. But if somebody's been in the ICU for a week and starts developing this weird symptoms, is it useful to send troponins or when do we win? So you had ST elevation, you want to see troponins, you really do want to know what's going on. So I think, yes, it's a love-hate relationship. I think you're right, though you can learn a lot more not by the presence or absence of troponin, but by the, right, by the cronicity versus the acuity, right? So the spike and fall versus that chronic elevation. So a lot of your patients, right, they're up, but they up the whole time they're here. They come back, I mean, they may come back in three weeks, six weeks later. They're the same level they wear then, you know? They just have this chronic leak because they have heart disease, but they've got whatever their underlying driver is that's causing them to present. But I do think that that spike and fall, you know, that acute malcardo injury, that's something that you can't pick up if you don't draw troponins. So I do think it's helpful for us to separate acuity versus crinicity. You know, our patient here was septic. And we, if this was a stress card myopathy, we thought it was due to the stress of sepsis, but people will also sometimes describe cardiomyopathy in sepsis as maybe an overlapping syndrome, but also a little bit of its own thing. There might be some specific factors related to inflammation and injury to the myofurbials and kind of, can you PC's apart at all? I mean, do you look at these separately or is there any kind of clinical relevance to it? More a research topic or? So you're right. I mean, a 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. We looked 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, you know, 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. So the picture you'd expect in the septic patient might be a little less sudden, maybe less rapid to improve as well. It might be less of a regional distribution on their echoes, but I guess you would just have to follow and see what happens, right? I mean, they are going to follow their own clinical course. It's not necessarily a specific treatment or anything. Yeah, I think you're right. And it's, like you said, it's almost always global. And unfortunately, they have usually a whole long laundry list of comorbidities that they may never recover that function because it's due to these other things, right? The diabetic, the liver, the kidney, et cetera, et cetera. All right. The other thing I wanted to ask you, we kind of glossed over it, but you mentioned hormone replacement therapy, which I assume you mean estrogen therapy in these older women. Does that reduce the risk of this? I mean, we talked about there's a risk in being postmenopausal that seems like it must imply that there's a hormonal mechanism here. And it sounds like if replacing it must help, but can you talk about all that? So I would love to say that replacing it must help, but we don't have that data. So it definitely was prefaced by the controversial comment that we don't really know. But I think each individual woman, you should discuss those things. There are some people who have their postmenopausal and they have marked symptoms. My suspicion, this is only my suspicion, that those patients probably would benefit more of a hormone replacement. We don't really know right now which patients, but this went through a decade of fear where all cardiologists knew, oh my God, you can't replace estrogen replacement therapy because you make their cardiovascular risk and their lipid profile is worse. We've learned that's just nonsense and that we've probably gone so far away from offering hormone replacement, estrogen replacement therapy now, that we sort of ignore that as an important treatment option. So it's out there, it's on the table, people are considering it and I think it's something that each person, you want to raise that as a discussion factor and probably treat some. But we don't have evidence to say that treating it makes it less. We do not have that. Right. We just know that after menopause your risk goes up, so we sort of are guessing that, I imagine this is being researched. It is, it's really fascinating, right? So in the US, it's the postmenopausal older female, but in the Japan, right? It's actually middle aged men after physical exertion that gets stress cardiomyopathy. So it's a whole different geographic world presentation. So there's so much about this disease I'm fascinated by that we just do not have answers for. My hope would be that as we study this and we begin to understand the mechanistic principles behind it, we can use it as treatment options for other things. I mean, whatever is happening here is it's guiding the myocardium to sit back, wait and recover later for whatever reason. How cool would that be if we could control that pathway? So, so I am fascinated by this disease, but I'm also the first to say we don't know much about it. Well, it is interesting. And I think, you know, to underscore the point, I think if we look, if you're looking for it in the ICU, you're going to find it a lot more than you think. And so I think that's one of the big takeaways here. All right. Well, thanks so much for joining us. I hope everybody found this as entertaining and informative as we did. We will throw some stuff up in the show notes, some links to some of the papers that Dr. Cheryl mentioned. Anything else you have parting thoughts or anything for us? No, just keep your eyes out there for it. And again, are they sick? Are they not sick? Do they have outflow track obstruction or not and go from there? Good luck. All right. That'll do it for us today. Remember, the opinions expressed today are just our own. We do not represent any of our affiliated institutions. And are just meant as general educational content, not specific medical advice. We'll talk to you guys next time. Thank you. Bye. ♪♪♪