These authors show us something very interesting about “negative” troponin testing in their prospective review. Like my facility, they had an assay with a certain level of detectability. I will say, though, that their assay detection level of 0.20 ng/mL is different than our assay, that goes down to 0.02 ng/mL. But, basically, they implemented a new assay that was sensitive down to 0.05 ng/mL but didn’t tell their clinicians any of the newly detectable troponin numbers below 0.20, but they built a database of the cohort in that detectable-but-previously-undetectable range. Then, they showed clinicians their new detectable numbers and let them do what they wished with it. It turns out, the population with the 0.05 to 0.20 troponins had similar cardiac morbidity/mortality risk as their >0.20 troponin population – while the truly undetectable did much better over their 1-year follow-up.
Additionally, after the new threshold was introduced, clinicians treated the 0.05 to 0.20 more similarly to the >0.20 group with additional testing, cardiology consultation, and medications – and their outcomes improved 20%.
So, this study really makes you think what it means to have a “negative” troponin and wonder what the disposition and follow-up should be at different points. At my institution, we’ve traditionally said 0.10 ng/mL is the cut-off for “positive”, and the lesser, yet still detectable troponins, are “negative”. But, this study clearly suggests that a lot of the patients we’re labeling “negative” really need to have more aggressive treatment. This study doesn’t tell us whether they need to be inpatient, or have expedited follow-up, or precisely how to manage them in order to improve their outcomes, but it suggests a lot of great new questions to ask regarding how to use the information we receive from our troponin assay.