19 Jan 2021
Frank Peacock, emergency physician and vice chief of research at Baylor College of Medicine, discusses the importance of cardiac troponin as a biomarker for myocardial infarction, highlights the benefits of high-sensitivity versus contemporary troponin assays, and shares why point-of-care testing is a powerful tool in the emergency department.
I am Frank Peacock, an emergency physician at Baylor College of Medicine where I'm the vice chief for research. My role in the emergency department as the vice chair for research is that I am responsible for all the research activity that occurs in terms of education and in terms of process of actually completing data gathering and all the other aspects of research.
So cardiac troponin is a critical biomarker for acute coronary syndromes which is the spectrum of heart attack for a couple reasons. First off, it defines the disease. That's how we determine you've had an MI or not because your troponin is elevated. And that disease is one of the most important diseases that appears in emergency departments.
It represents about 10% of all emergency department visits. There's nothing higher than that. And coronary artery disease is the number one killer of Americans. In fact, it's the number one killer of everybody in the industrialized world. So it's the most common, and the most critical presentations are all defined by troponin. So the challenges of detecting myocardial infarction really are going to stem around what kind of troponin assay do you have.
The first feature is that nothing makes a troponin go up like a myocardial infarction. Lots of things. The troponin is a structural protein. If it is out in your bloodstream, it's because some part of your heart died. And a heart attack is a big death, but other things can kill your heart, too. Not so big usually.
Nothing really makes a troponin rise like a myocardial infarction does but smaller elevations are critical, too. And so the challenge comes is how good is your test. If your test... I'm going to make up some numbers for you. Let's say your test can only detect levels greater than 100 and you come in and your level is 40 and then it's 60 and then it's 80.
That's a really fast rising troponin, and your assay can't detect it because it can't detect it till 100. And so what you have to do is hang around there until it gets above your level, and that's why we do serial levels because our assays aren't very good and you're waiting for it to go above that number that it can detect that. The new assays can detect down to 3 or 4.
So if you do an assay and an hour later do another one and it's not moving, you're done, but the old assays are terribly blind. They can't do it. So contemporary assays have people hanging around forever. Doctors get this confused all the time. High-sensitivity troponin does not give you better diagnosis of MI because the old assays diagnosed MI, too.
What high-sensitivity troponin does is allow you to know when they're not having an MI, something that contemporary assays simply cannot do. You've heard me say that troponin is my favorite molecule, and my favorite test strategy is point-of-care because, as an emergency doctor, troponin is the most important molecule and point-of-care is the fastest way to do anything.
And historically I've published and studied point-of-care for years. Point-of-care is outstanding and it's quite clear what it does. Point-of-care speeds everything up by about an hour, and we've done large studies on that where we handed the patient a stopwatch and, when I knew the troponin result, I click the button and we said, "Aha! How long did that take?"
The average was an hour if we did point-of-care. If it was sent to the central lab, the average was two hours. So it buys an hour. And if you're a normal person, an hour is a long time to be sitting around in a hospital gown in an ER worrying you're going to die. That hour is important. It's also important for me who's got a crowded ER who can send you home if it's negative.
And so that's what point-of-care gets me. Now the sad part of this question is, "What about high-sensitivity troponin and point-of-care?" The unfortunate reality is that it's not in the market currently. We hope it to be because it would revolutionize what we do currently, because we've been caught between a rock and a hard spot. Historically when we had contemporary troponins, we used point-of-care troponins because they were as good as the lab.
None of them were very good. The patient had to stay around forever, but if we did point-of-care, they got out an hour earlier, then high-sensitivity comes. Now patients can go out in an hour. Point-of-care cannot keep up. So point-of-care has been left behind with the tidal wave of high-sensitivity troponin coming. However, as soon as we get point-of-care that has high-sensitivity characteristics, it's going to be back in the game once again saving us an hour on every single patient.
And if you do the math on this, about 50% of the patients can be discharged with high-sensitivity troponin on their first or one-hour blood draw. If you do the math, that's about something on the order of 5 million patients a year could be discharged 1 hour earlier from the emergency department. That's 5 million hours of ER care.
That's really important and stresses the reason why emergency doctors think point-of-care is the best thing ever; it's because we run departments where we discharge people and if we can't do that, our departments get full and the we don't give good care because they're too full for us to do quality jobs, so it's critical that we do things quickly. So when high-sensitivity troponin is brought into a system, there is an impact to resources and patient care.
But it's not what everybody is worried about. We have data on this from Europe where, because they're 10 years ahead of us, they've evaluated this in a before and after model. They have a system that can measure length of stay and costs and numbers of caths and then bring in high-sensitivity troponin and measure that all again and see what the impact is.
That's been done in multiple hospitals. And what you find is that the cath rate goes unchanged but the diagnosis of disease goes up. So they quit cathing people who don't need it. That's a plus. In the emergency department, stress test usage goes down, length of stay goes down, and overall cost goes down. Also a plus.
So if you look at this from a system perspective, it's the business rule of better, cheaper, faster, you can pick two except, in this situation, you get to pick three. It's better because you're identifying the right people who get cathed and getting rid of the wrong people who shouldn't be cathed. You are discharging people at a higher rate with lower length of stays and at less cost to the system.
So it's a big win. The concern that you're going to have more diagnosis of MI, more testing has not been borne out. In fact, the exact opposite is true.
Baylor College of Medicine
Dr. Peacock is a professor of Emergency Medicine, associate chair, and research director for Emergency Medicine at Baylor College of Medicine. With over 300 publications on heart failure and acute coronary syndromes, Dr. Peacock is also the co-editor of the textbooks Cardiac Emergencies, Short Stay Management of Heart Failure, and Short Stay Management of Chest Pain. He is the 2004 and 2010 winner of the Best Research Paper Award from the American College of Emergency Physicians, and is the Codman Award recipient from the American Association of Group Practice. Dr. Peacock has and continues to serve as PI or co-PI for many high profile national and international clinical trials such as PRONTO, ADHERE-EM, IMPACT, CHOPIN, CLUE, FASTTRACK and TRUE-HF. His clinical interests and research focus include acute coronary syndrome, acute heart failure, biomarkers, improvements in emergency medical care, and more rapid patient disposition. Dr. Peacock received his medical degree from Wayne State University Medical School and completed his Emergency Medicine training at William Beaumont Hospital, Detroit.