INTERVIEW
Practical Advice
for Clinicians on the
Imminent Arrival of
hs-Troponin Assays
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,
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
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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
James Januzzi, Jr., MD
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 he