Practical Advice For Clinicians on the Imminent Arrival of hs-Troponin Assays
Interview | Measurement of troponin has become a highly sensitive issue in the last few years. While we don’t have an assay approved yet in the United States, approval may come later this year or next year. So, what should physicians expect when measuring highly sensitive troponin? A recent issue of JACC discusses this issue in an article titled “Implications of Introducing High-Sensitivity Cardiac Troponin T Into Clinical Practice.” Providing some practical advice based on this publication, is James Januzzi, Jr., MD, FACC, the Roman DeSanctis Scholar, Clinical Scholar, and also a Professor of Medicine at Harvard, as well as the Scholar at the Massachusetts General Hospital.
CardioSource WorldNews: Let’s begin by talking about SWEDEHEART Registry. Can you give us some background on it?
James Januzzi, Jr., MD: The SWEDEHEART Registry is an interesting and very large data set. Basically, in the country of Sweden, there is a centralized data repository that can track the course of over 40,000 patients admitted to the hospital for various diagnoses. We just published a paper in JACC Heart Failure, for example, looking at the experience from SWEDEHEART with heart failure patients. In the JACC study, the authors used the SWEDEHEART Registry to look at patients admitted to the intensive care unit or similar setting for suspected acute coronary syndrome.
Now, what did they find in terms of the data?
Well, I think it’s important to emphasize that the idea behind the study was to ask the question, “What has been the practice patterns around these patients, the final diagnoses of these patients, as well as the prognosis of the patients?” Because there’s still some open questions about what highly sensitive troponin will bring.
What the authors found was that a substantial percentage of patients had very low values for highly sensitive troponin. Interestingly, in this study, some have previously suggested that patients with very low values—in other words, those below the detection limit of the assay—could potentially be rapidly triaged, because they’re unlikely to have acute myocardial infarction (MI) or unstable angina. What they actually found in SWEDEHEART data was that that wasn’t the case; there was a measurable number of patients with very low, highly sensitive values that, indeed, had an acute coronary syndrome. So that’s an important point.
On the other end of the spectrum they found, as has been shown, that highly sensitive troponin reclassifies patients from unstable angina pectoris to acute MI in about 20% of cases. The newer troponins are more sensitive than the older ones in finding these patients, but there was a substantial number of patients that had an elevated value for highly sensitive troponin who did not have an acute MI. This proves to be a cautionary tale for clinicians when we start testing.
When I looked at this article and saw that the subtitle included some practical advice for clinicians, my immediate thought was that this could be one of the best-read pieces in JACC for the year. Seriously, this has caused a great deal of controversy and consternation. In this country what should we expect, and what practical advice can you give?
Yes. It’s an incredibly important topic because we use troponins all the time, and when we are looking at these patients we are carefully watching for the presence of MI—particularly because that has a defined treatment strategy. What we can tell clinicians is that, when we shift to the highly sensitive troponins, we will be able to, in a much more rapid fashion, identify or exclude necrosis of the myocardium. There are data showing that, within 1 to 3 hours, a patient can be successfully completed in their rule-out or rule-in. So, unlike older troponin assays, the decision might be earlier, which is nice.
However, because of the increased sensitivity, we now recognize that there are situations where myocardial necrosis occurs outside of an acute MI that we never detected before.
In this editorial, I provided a figure from the universal definition of MI Task Force Document that really illustrates how clinicians should be thinking about troponins. They’re no longer to be thought of as a heart attack biomarker. They should be thought of as a myocardial injury biomarker. So, situations like myocarditis, hypertension, heart failure—things that are not heart myocardial infarction per se—will be picked up with these assays. But, another very important point for clinicians to recognize is that the SWEDEHEART investigators found that regardless of gender or age, if the highly sensitive troponin is elevated the risk for the patient was higher. Almost truly independent of the diagnosis, patients didn’t have to have an MI. If the highly sensitive troponin was high the patient’s risk was considerably higher, which really says that we need to pay attention to why the troponin is abnormal and not just say, “Ah, it’s not an MI. Let’s just discard that elevated value.”
I know a lot of centers have been trying to get people processed in and out faster and faster. This finding will really be helpful to patients as they will know sooner and not have to wait hours for some determination.
We know—and again, we have the benefit of knowing from the European experience—that one may be able to successfully complete the process of ruling in or ruling out within just a few hours. The data for highly sensitive troponin show that patients are more often than not positive at presentation, and soon after presentation. One recent study, called the TRAPID-AMI Study, showed that within 1 hour you can see a significant delta, a significant rise in those patients destined to have an MI. So, by using a rapid rule-out or rule-in strategy, three quarters of patients can have a disposition within an hour.
That’s got to remove some stress from the patient, because it’s not a happy thing to be in the hospital in the first place if you’re wondering whether you had a heart attack.
Certainly not. And it also adds a lot of relief to the emergency department setting in terms of making decisions, whether a patient should or should not be triaged in or out.
I think, if anything, the initial reaction from cardiologists will be somewhat of concern, maybe frustration, because now we can see things that we hadn’t seen before. However, you talk to the Europeans and they say, “Do not take this away from us. We love it. We’ve learned a lot, and we’ve changed our practice styles because we now can detect things that we weren’t able to before.” That can only improve care in the end.
Melki D, Lugnegård J, Alfredsson J, et al. J Am Coll Cardiol. 2015;65(16):1655-64.
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