Figuring out the value of a troponin measurement is both simple, and complicated. Big numbers are still straightforward and trouble. Small numbers – and even smaller still – are increasingly difficult to parse.
What does seem to be true, at least: the closer to zero, the better.
This is a multi-center evaluation of a 0- and -1hour troponin delta strategy, based on a hs-cTnT from Roche. These authors prospectively enrolled 1,458 patients with chest pain of peak intensity within 6 hours. Samples were then taken at 0, 1, 2, and then at least 4 hours after presentation. The outcome of interest was an independently adjudicated final diagnosis of acute myocardial infarction. And, this study probably shows just about what every similar study has shown: initial sensitivity is ~90%, with marginal increases as additional time points are added, while specificity suffers predictably due to the nature of the assay.
However, there are a couple concerning potential sources of bias. The authors enrolled 1,458 patients – but exclude 176 of them from analysis for a variety of reasons. In a study trying to catch rare events to demonstrate near-100% sensitivity, over 10% of patients dropping out is an important consideration. There were also issues with slow enrollment, compared to previous studies, and the patient flow diagram is extremely sparse. Over two years, the centers involved likely had many thousands of chest pain presentations. No information regarding the missed enrollments is presented.
There are also issues with the adjudication downstream, which was based on the results of various follow-up examinations as well as, oddly enough, a different troponin assay: s-cTnI-ultra. 213 (17%) patients received a final diagnosis of AMI, while 167 (13%) received a diagnosis of unstable angina. The clinical significance of their definition of unstable angina remains unclear to me – myocardial ischemia without cellular injury associated with chest pain at rest. The authors reference these UA patients as being at low risk for poor long term outcomes, which seems clinically discontinuous with the sort of “critical near-occlusion” working definition I’m familiar with for true UA. Regardless, the safety of their strategy is only reasonable if UA is a relatively benign catch-all diagnosis for troponin-negative chest pain, so I will accept their categorization.
There were also diverse and perverse conflicts-of-interest described with the manufacturer of the assay involved.
Regardless, as previously stated, these data are consistent with prior demonstrations – so, yes, using these assays at presentation, or as 1- or 2-hour deltas in the Emergency Department, will result in a very low miss rate when paired with low pretest likelihoods of disease. Furthermore, anything missed by these assays will be such a minute injury pattern as to be extremely low-risk for short term cardiac mortality.
Yes, Virginia, you can discharge chest pain.
“Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T”
http://www.annemergmed.com/article/S0196-0644(15)01501-2/abstract
I am a medical student. So this post really help me ! Thanks !