Episode 12: The New Troponins: A Highly Sensitive Topic

Join our host, Drs. Ben Alencherry and Andrew Hornick, along with Ohio-ACC President  Dr. Kanny Grewal, clinical cardiologist from OhioHealth Riverside Hospital, as they discuss the practical use of high-sensitivity troponin assays. They review the key differences of the new assays, their role in diagnosis and risk stratification, and tips for transitioning from prior assays.

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For more information, see the 2019 Scientific Expert Panel for Transitioning to High-sensitivity Troponin from ACC.

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Please subscribe to receive updated episodes automatically! Visit https://www.ohioacc.org/cardiohio-podcast/.

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Transcript

0:07

Welcome to the Cardio Ohio Podcast, a production of the Ohio Chapter of the American College of Cardiology. This is Can Greyal in Columbus, Ohio. This is Ben Allen Cherry Cardiovascular Imaging fellow from Cleveland, Ohio. More information on the podcast, including past episodes, is available@ohioacc.org. And now for today's,

Ben 0:33

All right. Hello and welcome everyone. This is I believe, episode 12 of the Cardio Ohio podcast. My voice is obviously new to the first speaker because we've flipped the tables. And K Graywall who is the co-host of the podcast, along with myself, is gonna be our. Now before I introduce him as our guest speaker, I want to take time to introduce Andrew Hornick, who will be stepping in Kenny's shoes. Andrew is a cardiology fellow from Ohio State. We did residency together at Case Western. Andrew why don't you give us a one liner, introduce ourselves to OU and and some of your interests. Hey,

Andrew 1:15

thanks Ben, and thanks Candy for having me on. I'm, a a second year fellow at Ohio State. I've got an interest in non-invasive cardiology and, and hopefully a focus on sports cardiology as well. I was born and raised in the great state of Iowa, but made my way out here for residency in Cleveland where, where I'm at the illustrious Ben Allen Cherry. So really great to to be here with you too.

Ben 1:37

Awesome. Thanks. Thanks Andrew. And before we reintroduce Kenny as the guest, we want to talk about our, our subject matter. And it's a different sort of subject than we've spoken about before. We are gonna talk all things high sensitive, each proin today, and we're gonna try to answer some of the common questions that people have. Kenny is a, is a content expert and has dedicated a lot of his. Research and clinical thoughts to high sensitive troponin and how it should be rolled out and how it should be used. So first I wanna, I want to reintroduce k k. Why don't you just tell us a little bit about how you, how you jumped into the high sensitive troponin field.

Kanny 2:18

Hey thank you very much Ben and welcome Andrew. Great to have both of you to chat with. Yeah, this is a little bit different hat for me than my normal hat is the president of the ACC and is a cardiac imager here in Columbus. But I really think this is an important topic. You know as you may know, Ben, there was just a, a report in, in j a C in the last couple weeks that showed that only about 30% of hospitals in the US have transitioned to high sensitivity. Troponin assays, even though they've been clinically approved for several years. My interest in this, and this is actually a good lesson for you fellows and other trainees back in 2017 when the first troponin T assay was about to be approved in the us We were here at Riverside Hospital in Columbus. We were approached by our, clinical laboratory team and the lead pathologist about, transitioning from the current assay. Proponent T over to the fifth generation or high sensitivity assay. They came to one of our department meetings and of course, we're extolling, the benefits of higher sensitivity and the results from Europe. And of course, as you can picture, this was a room full of cardiologists. The first reaction was, what the heck are you guys doing? We don't need more sensitivity to our proponent. We don't need more cardiology consults. We don't need more false positive diagnoses. So then I spoke up and I proposed a suggestion. I said, before we transition to this new assay, why don't we study it ourselves in our own? Patient population. So I suggested that we take the new assay and we run it simultaneous with the existing assay, the fourth generation on a group of patients, and then look at how it performs clinically in terms of outcomes to help guide how we're going to implement it. And of course, everyone looked at me and said, Hey, that's a great idea. Let us know how that works out when you do it. So suddenly I became the position champion for. Transition to high sensitivity troponin. So that's the lesson for you guys, which is if you decide to speak up at a staff department meeting, you may find yourself taking on some new tasks. But nevertheless we, we, we then actually did that. We did a study where we did both essays on the same samples in many thousand patients over a three month period. And I presented that research at the a ACC meeting at that time, which I think was 2019. And ever since, I've been kind of teaming up with our. Little team to continue to explore like how the assays working in terms of, delta troponin accuracy for events, trying to figure out optimal cutoffs, et cetera. So it's been kind of an interesting journey and we're now several years in and, and still kind of learning the process. So that's, that's kind of how I came to be a troponin guy.

Andrew 5:14

That's awesome. And I, you know, I think as a, as a cardiology fellow, certainly from time to time we've waited through lots and lots of positive troponin consults. I'm curious, I suppose, could you define just for us and for the audience, maybe the, the definition of a high sensitivity troponin, how that differs from some of the older generation assays

Kanny 5:33

yeah, sure. So of course you guys are too young to remember, but there was a time back in the early days where diagnosed with myar infarction was pretty challenging because we were using multiple biomarkers, things like C P K and. ldh, even all kinds of crazy stuff. You know, you would get a panel and it was just this crazy scheme to try to figure out what was positive or not. Troponin came out, I think, in the early nineties, and of course there's been successive generations of the assay. Just as a reminder to everyone, remember that the troponin complex is, unique to heart muscle. And the troponin complex actually has three proteins or subtypes troponin, t i, and C. But the actual assay for the is, is based on either troponin T or the troponin I sub components. And so the subsequent generations have gotten better at detecting the protein, of course is so helpful in cardiology because troponin. Almost completely unique to heart muscle. Apparently there's very, very tiny mouth of troponin T and skeletal muscle, especially when people have skeletal muscle disorders, you know, rhabdomyolysis and some of the inherited muscle diseases. But basically it's unique to the heart. So any detectable level of troponin. Pretty much implies cardiac injury other than the exception of slow clearance, you know, in renal disease. Part of the issue with previous versions of troponin, like, the existing troponin t that was used previously is that it, it, it didn't pick up low levels very well. So actually the 99th percentile cutoff was actually higher than the detectable cutoff. So basically any. Any detectable level by the assay was considered positive, and that's how we, treat a troponin in the past. So, high sensitivity just refers to the fact that these newer assays can actually detect circulating levels of troponin that are below the 99th percent. In other words, they're quote normal and I, if it can do it with a certain accuracy, which we call the coefficient of variation, then that meets the threshold for being called high sensitivity. Now, There is a difference between troponin T and Troponin I assays. The troponin I is made by many different companies. And each of the assays that's used for T trop I is slightly different cuz they use different antibodies. These are all antibody assays. So troponin I is in the public domain so anybody can make an assay for it. So as a result, there's multiple troponin I assays and they're not interchangeable because they all use slightly different antibodies and different methodologies, whereas troponin t. Is proprietary. It's only made by a single vendor, which is Roche from Europe. And so Troponin t being proprietary, it's a, a single assay that's more interchangeable between institutions. Now we at Riverside use troponin t I believe you do at the clinic as well. So a lot of institutions do use troponin team, but there are high sensitivity troponin eye assays as well. It's just that there's a little bit more variability between those.

Ben 8:44

We, we definitely use troponin t I haven't seen many troponin eyes.

Andrew 8:48

But you know, I think it, it is certainly the, the circumstance where every once in a while you will get a patient transferred to our institution who is coming with the, you know, a different troponin assay in their chart, in their lab.

Kanny 9:00

In fact you know, you guys probably see this at your institutions too. You'll see these patients transferred as a quote non-St. STEMI because of bedside troponin at an outside ed or whatever was elevated. And then of course, you repeat the markers at your own institution and they're negative. It's really a problem with older assays, with troponin and I, especially the bedside ones because they use a different methodology and there's more cross reaction with other proteins in the blood. At least with the newer generation, whether it's i r t, it is more specific, but of course it's also very sensitive so you can pick up low levels.

Ben 9:37

Yeah. And Kenny, that that sort of background information is very important. It kind of sets the stage for this to what you kind of brought up, this higher sensitivity. Picking up myocardial damage earlier. Like what does it mean clinically that you've seen in that we are probably picking up a lot more Type two mi. And just for the, for the background audience, you know, type one we think of as as acute plaque rupture or acute coronary syndromes that are occurring. There's primary blockage of the heart artery type two. It's more a supply demand problem. And this is me oversimplifying it, but just for a general schematic, do you think we're picking up more Type two mi. And, and in Riverside, as you've seen this been being rolled out, how have you navigated that, like teaching cardiology fellows helping other practitioners navigate a mildly positive troponin in the wrong clinical setting in that it's not an acute cornea syndrome?

Kanny 10:34

Well, it, you know, it's a challenge. Of course with any test that you are all, whatever cutoff you pick as quote, abnormal is a trade off between. Sensitivity and specificity, and that's the case with troponin. Of course, the forte of the assay is how sensitive it is for very, very low circulating levels. So of course you are gonna pick up smaller amounts of injury. The important teaching point though is that any, any detectable troponin, especially if you detect a serial change, And the levels is consistent with injury, you know, even if it's a low level positive that is cardiac injury occurring, it's just that cardiac injury can occur for lots of different reasons besides obstructive CADs and you know, thrombotic or type one mis a as you alluded to. So, the way, a couple other things to point out about the assay is, is, each institution does set its own cutoffs. You know, there's some recommended ones from the vendor, but. One of the big differences with trope T at least, is that there's different cutoffs for men and women. And, and this is something that they kind of learned in Europe as they were using the Asay more widely, is that, women who have less overall total myocardial mass will have lower levels of troponin release with injury than Manuel. So if you have a single cutoff for both sexes, you're gonna basically over detect. Positives in. And under protect them and women. In other words, it's gonna be less sensitive than women and a little bit less specific in men. So we at Riverside decided to go with sex specific cutoffs. So we use a cutoff of 22, you know, nanograms per liter in men and 14 in women. I think most institutions do that, but I don't think everyone does. I think there are some who use a single cutoff because it's just easier for clinicians to, and kind of interpret. But we did go with sex specific cutoff, so that does help a little bit because that helps, you know, pick up fewer false positives in men and it makes the Tesla more sensitive in women, but it's still a trade off. And as you alluded to, With such a sensitive assay, you are gonna have more types of cardiac injury that are due to other causes including type two ischemia, but also, you know, many other things that all of you guys know about as, as, as other causes of cardiac injury, like sepsis and pulmonary emli. Other coronary issues like hypertrophy you know, accelerated hypertension AFib rbr. And we do see more of that, there's no doubt about it. Now, one thing we do to try to mitigate that is we report the Delta troponin as an actual result with a normal value or abnormal value to help our clinicians. So when people get serial troponin, we actually decided to report the Delta troponin as a value. And we arbitrarily have picked 20% as a, as a clinically significant cutoff. And so that helps our clinicians so that if there's just a flat elevation with a negative delta, the interpretation actually says that this could be chronic injury. Rather than acute ischemia. So that helps reduce, the cardiac testing and hopefully reduce some of the consults we get for elevation, because as you guys know, you can have flat elevation and a lot of chronic cardiac and non cardiac conditions. So those are the kind of things we've done to try to. Kind of find the balance between sensitivity and specificity. But we actually just presented an abstract at the ACC two weeks ago looking at that exact question you asked Ben, which is how often do you get, troponin elevations that are not due to obstructive c a d. And we found that the incidents of Manka, which is, you know, myocardial infarction with normal coronaries was actually about 25%. Since we've started using HS troponin, whereas in the typical literature, you know, 10% or less. So I think we do have actual evidence that we're seeing a lot more non-ischemic type elevations. But the key is that it really is cardiac injury and, and it really indicates a poor prognosis. It just happens to not be due to obstructive disease. So it's still worth, diagnosing that injury and using whatever tools you have to exclude, obstructive.

Ben 14:47

And before we we jump topics real quick. You had said that your hospital provides the delta troponin number, so along with like the second high sensit troponin value, it will actually provide the delta. Is that correct?

Kanny 15:00

Yeah, and what we did is we used 20% is what's considered a significant delta, but below 28. Which is we use an absolute change of seven. So our criteria for a positive delta is that it's an absolute change of at least seven or 20%. You know, whichever's higher. Cuz obviously if somebody's troponin goes from eight to 10, that's a 20% change. But we all know that's not really clinically significant cuz those are normal levels. So we use a delta for the percent, for the higher numbers and absolute change below, but we actually do report it. And, and in our laboratory result, there's actually a little interpretation guide that explains, when it's significant or when it's not. Try to hopefully minimize consults

Ben 15:43

Yeah, the battle is just, it's just conveying that new new topic, new education to all the providers. Cuz you can't expect, like ed providers, general medicine providers to stay up to date on these new literature when, when even cardiologists sometimes are trying to keep on edge. So that, that seems like a novel

Kanny 15:59

way. Yeah, absolutely. You know, one of the big roles for us, Cardiology consultants, of course, it's easy to sit back and complain about, the silly consults and all those things. But, educating hospitalists and educating emergency room providers, that's gonna fall on us as cardiologists. We're kind of the gatekeepers for these issues. So part of our rollout included a lot of education and it wasn't just one time, it was ongoing with our hospital. Our residents and our ER docs, so that's definitely been a big part of it, be of any plan for any institution that's planning transition.

Andrew 16:40

No, I, I think along those lines one of the things that was exciting about high sensitivity troponin at its rollout was its utility to be a rule out test for patients come into the ED with chest pain. Has your institution you know, added any sort of risk scores or risk calculators, like, you know, heart score or something to your to your algorithm in the ed? And is that something you talk about with the providers, how to use the high sensitivity troponin in addition to those

Kanny 17:06

scores? Yeah, absolutely. In fact, we're big proponents of heart score as well. I like heart score because it's just so simple and it's great for a non cardiologists. You know, most cardiologists can look at a patient and say, gosh, you have St. Depression, or you have these risk factors. We know your elevated risk. It's pretty obvious, but. It's not so obvious for hospitalists and, and er docs. So the heart score is a great tool because it's so accessible and simple to calculate. So we actually advocate that for every patient that it, that the troponin be used in conjunction with the heart score. And as you alluded to Andrew, one of the biggest values of the neway is when it's totally normal. I mean, that is such a low risk patient that you feel very confident that you can discharge them and avoid bringing'em in for testing. And that's something the cardiologists don't often see. You know, we see the unresolved of the ones who get admitted and get the consult, but what we don't. Is, and I didn't realize this till we did, looked at our own data, but about 90% of chest pain patients in most eds do get discharged. You know? And having that undetectable trope is like so, such a confidence boost because the data, the literature shows that that's just an extremely low risk patient. But if you combine it with a lower risk heart score, it's even lower risk. And if they're in that low risk heart score group, there's plenty of data showing that like the 30. Event rate is, is just microscopically low. And so those are the patients you can safely discharge with having to bring in for observation. So I think that's been one of the big benefits. And I think any institution that switches over is gonna see that a lot of those low risk admissions start to disappear as you get comfortable with the asay.

Andrew 18:45

I'm curious about how you, how you might approach along those lines in the ed. You know, a patient who comes in with maybe something that, that sounds like typical chest pain and has a troponin value that is less than that 99 percentile cutoff. But does follow some of the kinetics that might be more classic with, you know, concerning for mi I think you said you, your cutoff value is about 22, so maybe their component goes from five to 20 and then back down to five another three hours. Do you have an approach for those patients or kind of a sense for what that might represent?

Kanny 19:15

It's really hard to say you know, obviously, You know that that 20 value would be high in a female. It happens to be just below the cutoff for a male. I think when you see that, of course, you know you know, one of your early questions was how do you balance sensitivity, specificity? Of course, when you're talking about chest pain patients, we all have to value sensitivity more, right? Because there's such a penalty for missing a myocardial infarction that you probably want to compensate for that in terms. Occasionally getting, you know, admitting somebody who turns out to be false positive. So, you know, I think in that kind of situation, you gotta err on the side of safety and say, well, you know, even they didn't peak positive. You know, let's look at their heart score. Let's see if their EKG changed at all. If there's any doubt, we'll bring them for observation and, repeat the assay or, or consider doing a noninvasive test. So I, I think because we gotta err on the side of, of not missing mis, we just have to, you know, accept the fact that you're gonna occasionally, Bring in patients that have negative workups, but I, I mean, that's been the story of chest pain as long as there's been chest pain, which is you don't wanna miss the infarctions. And of course there's other tools like I'm sure you guys use at your institutions that can really help, like C C T A, you know, you can do C C T A directly in the ed and it's a great tool for these kind of borderline cases that maybe you don't want to necessarily admit or put through a big workup. Because once again, a negative CCT is almost a hundred. Negative predictive value for, for disease. So such a great tool. Even a calcium score, honestly, there's data that just a negative calcium score alone has predictive value. So I think those are the patients who probably end up needing some of those tools,

Ben 20:57

and just a quick plug episode one of our podcast talks a little bit about some of these non-invasive imaging modalities. I, I just wanted to bring us back to, first of all, like back in the day when Andrew was a, was a young intern and I was actually his chief resident, and that might explain some of the negative stuff he's gained. So I apologies that Andrew, but we learned a lot about this thing, unstable angina, which was like the bane of all our existence. When you're the resident overnight and you admit this patient with chest pain and the Ed's like, well, he's high. And you know, things are negative, but it might just be like we're not catching it. What do you think, and this is like an existential question now, do you think unstable angina exists anymore in the era of high sensitivity troponin? Well,

Kanny 21:41

you, I, I'm sure you remember that when we talked about unstable angina, whether it was recently or even back in the day, we were probably talking about a group of disorders, right? I mean you think about the patient that you see in clinic who says, gosh, doc, you know, I, I, I've been working out and I get this little tightness in my chest now that didn't used to get, maybe it's even a patient with known. I mean, you know, a patient like that's not gonna have positive cardiac markers, but technically if their chest pain's progressing, then it may be quote unstable. And those patients still exist. And of course a lot of them end up getting stress tests and cats and have obstructive disease and need treatment. In the emergency room setting though, I think unstable angina has gotten much less because so many of them now turn positive, With Hs troponin, at least a troponin t we use the with the old, old assay, we considered a positive 0.04 or higher 0.04 nanograms per milliliter. Well, that, that corresponds to a troponin T of 50. So if you think about it, if you could only detect proponents that were 50 or. Think about all those, non-St. STEMIs and other ones that, that we now pick up that, that we would've labeled unstable angina back in the day. And there's a lot of them. So I think they're, they're transitioning over because of the asay, but, but it's still exists.

Ben 22:58

Yeah, I think that's a, that's a good point. And you know, one thing we always talk about is that even stable when it first starts is by definition unstable. So I, I think it's, it's not just from my experience, it's just cuz we have these new biomarkers doesn't mean we ignore those patients who are enzyme negative, but have stories that sound. Somewhat worrisome and they have risk factors. You know, I don't think that's okay. Never see the cardiologist again. It might just be an opportunity for strong primary prevention and close follow up. Andrew, you wanna, you wanna take us to the, to the next Jack paper? Yeah,

Andrew 23:36

definitely Ben. And, you know, despite, despite what Ben says about our checkered path, you know, he was, he was quite a good chief resident. I gotta give him, I gotta give him props, I guess, for that. Even though he is, you know, a Maryland basketball fan. But you know, I think part of the, I think part of the. Genesis for this podcast topic was the, was the recent article in Jack. And you know, I think, can you touched on how, you know, the Ohio Health journey with high sensitivity troponins started kind of rolling it out in 2019. You know, how did the findings that you all had at your institution compare to, you know, the recent jack paper and do you have any comments on sort of the, the findings in that paper itself?

Kanny 24:15

No, I, I think it kind of reinforced what a lot of us have seen at, at institutions that have been using the assay, which is that kind of the fears that it was gonna lead to a lot of downstream testing were kind of unfounded, and it's just like what we were talking about before. I think there's, the thing about the HS assay, is that, when it is normal, you just have so much confidence that, that the patient's low risk and doesn't. Immediate testing that the, as the paper showed, a lot of, there's actually less testing gets done. I think it did show that there was a little bit more coronary angiography since the new as essay came. And that's probably because you're kind of picking up these these low level positive Because I think, you know, there's still a tendency to kind of fall back to angiography when you see an elevation, and then that's definitely not the case with this new assay. As, as over experience in time, we've learned that so many of these low level positives have non-obstructive disease that, you can definitely rely on, whether it's nuclear imaging, C C T. Et cetera to confidently rule out disease where they happen to go to a cath. So I think that's kind of the lesson from that paper, which is that we still need to reduce the normal cath rate. But it is reassuring, and this is our experience too, that there's not a lot more utilization going on, whether it's, you know, admissions or

Ben 25:34

testing. And as that utilization kind of gets wider, Kenny, one thing that we've seen is even in, in patients who have some form of C K D clearance of this, high sensitivity troponin can be delayed as we know. Do you have any guidance for when consultants call you, or primary teams call you about how to interpret high sensitive troponin in the setting of c k D?

Kanny 26:00

Yeah, I think there's definitely a couple strategies that help Cause it's a very challenging situation and, and it's not just even. Those patients, it's the patients with other chronic disease or critical disease in the units. One strategy is that the delta troponin still applies. So even if you have poor TR clearance due to renal disease, If there's a peak and a fall in the levels, that's still consistent with acute injury. Now there's still differential for that, of course that we have to think about. But so I think you can rely on the delta, a little bit of those patients, number one. And then number two is use a simple noninvasive tool like a bedside echo. And there's a lot of literature showing that the Echo's a great stratifying tool. So in patients who have, an. Cardiac marker. If you can document that the EF is globally normal and the Wal motion is normal, there's data showing that they have a good prognosis at least as far as, cardiac outcomes. So that's a very helpful bedside tool with, really not much of any risk really that can stratify those patients and kind of try to sort out which ones really do. Further evaluation or not, but no matter what, it's gonna be a challenge in most patients, and it's still a challenge with the new.

Ben 27:17

I think that's a great idea. Using like non-invasive testing like Echo to kind of help parse out those sort of patients who, even by nature, M C K D, they're at higher risk of having cardiac events in that same, in that same vein, we, as we were learning like 10, 15 years ago, We sometimes use CK and B which has fallen out of favor. Obviously, the role that we learned it in was re infarction, where while the troponin T was still on its curve of being eliminated from the body C K M B might be able to show another peak so that if you had a rein infarction or an early infarction after. I wanted to ask you, have you heard of any role for high sensitivity troponin in those settings of re infarction?

Kanny 28:02

Yeah, I, I, I think because it is so sensitive to injury, it's more useful than the prior assays in that setting. You know, the usual scenario, somebody who comes in with an MI and has a pci, they go home and then maybe five or seven days later, they're back in the er. With atypical pain. You're trying to sort out, is there really something new going on? I think in that setting it is helpful because even though it may persist for up to seven to 10 days after an mi, I think you will see a, a new rise pretty quickly if there's truly, stump thrombosis or something like that going on. As far as ccp, K and b, I mean, I'll have to be honest Ben, I think you were probably in grade school last time I went to CP k m. I was in diapers order

Ben 28:42

one probably, which hopefully wasn't grade school. That was the only bio marker he taught us.

Kanny 28:49

So if there is a utility pro and b anymore, I'm not that aware of it, but maybe people smarter than me have, have figured out a way to integrate it in. Kind of a along

Andrew 28:59

the lines of, you know the nuanced uses of, of the high sensitivity troponin and specific populations. Is this a test that you're ever using in the outpatient setting? Are there, is there a specific patient say, or patient population that you might find utility in it?

Kanny 29:15

Yeah, I think very rarely I would say I'm sure you guys would agree, but there's an occasional patient you see in clinic where you just park them in the waiting room and send off the trope tea. Cuz luckily we have a lab right in our clinic where I practice where we can immediately draw blood work and send it off. I haven't seen much utility in other conditions. Now, of course, there's a lot of literature showing that just even chronic levels of t trop. Can predict prognosis. So I think in a lot of conditions there's literature that it correlates with their prognosis. But but in terms of how you apply that to a given patient sitting in front of you, I'm not sure.

Andrew 29:53

Excellent. Thanks. And then I, I guess one of the other, the points that that this paper made and that you touched on early, earlier in our talk was that, still only maybe at one third of hospitals are using the high sensitivity lab tests. Do you think there are specific barriers that are present or preventing the uptake of this, lab specific factors? Or is it just kind of, you know, slow rollout and slow it out at adaptation to, to

Kanny 30:16

new. Yeah, I think some of it's just the inertia to change, but as I learned in our rollout, you know, it's a very complicated process to change these assays. It's not the same. It's simple as like, oh, we're gonna stop using this on December 31st and start using the new one on January 1st. You know, these, these laboratory systems are so automated that their million dollar. And, you know, you just don't change'em over overnight. So I, I think there's just a lot of, there's expense involved, there's education of clinicians and there's just inertia. You know, unless you have a physician champion who's kind of understands the literature and the utility, there's just gonna be a lot of physicians who are very comfortable with what, what they already know. And that acts as a sort of resistance. But I think as more and more literature comes out, it's very obvious that. You want to have the the best assay. I was at a talk once recently about troponin, and one of the clinicians was talking about how there's a saying that he was using, which is, back when Troponin was a terrible assay. It was a great test. Now that it's a great assay, it's a terrible test. And, and I disagree with that. I think that's, that's an old school view of that. But I think it's more of a issue of just understanding how to use it. And, and I think in that setting it's clearly, help helping us triage our patients properly.

Ben 31:39

Ken, and I think the only way that statement was true from the speaker was when you're the general cardiology fellow on call and you're not getting paid per consult. I'm not sure if I'm allowed to say that on air, but so we should wrap up. We are, we are very respectful of all our listeners' times that this is a round, 30 minute podcast. I wanna summarize, first want just thank Candy for, for changing his hats and being the content expert for this podcast do you have any last words for us?

Kanny 32:07

No, I think it was a good discussion and I thought you guys asked some great questions and unfortunately my consult list is getting longer, so I need to go going.

Ben 32:15

Yeah. That's great. And Andrew might be seeing some of these consults. Thanks a lot, Andrew, for coming on.

Andrew 32:21

Just thanks for, thanks for letting me join.

32:23

Thank you for joining today's podcast. For more information about the speakers or the topics, please go to Ohio acc.org,