I have collected several articles on the interpretation of hs cTnT/I. The interpretation of this new and ultra sensitive test can be very challenging in critically ill patients that have additional co-morbidity's, particularly in septic shock , ARDS etc...
Commenting on the ever increasing sensitivity and decreasing specificity of troponin assays, Robert Jesse crypt, "when troponin was a lousy assay he was a great test, but now that it is becoming a great assay is getting to be a lousy test. Recommendation however is is that frequent monitoring of troponin kinetics, along with careful attention to the noncoronary causes of troponin elevations we will keep the high-sensitivity troponin assays extremely useful markers for myocardial injury.
Data from the SWEDEHEART registry, points out that a large proportion of patients will have minor cardiac troponin increases the majority would do not have a myocardial infarction. However despite remaining a heterogeneous group be adjusted mortality rate start to increase at the level of the 99th percentile in healthy controls.
From BMJ February 2019: In the hospital population of 20,000 consecutive patients, 1 in 20 of all patients had a high-sensitivity troponin I concentration greater than the manufactures recommended 99th percentile. In most of these patients there was no clinical suspicion of acute myocardial infarction. In this particular study the 99th percentile of the high-sensitivity troponin I for the whole population was 296 ng/L compared with the manufactures quoted level of 40 ng/L currently used clinically as upper limit of normal for high-sensitivity troponin I.
Among patients with infection [ including the post-infection period ] there is also an increased risk of myocardial infarction. Pathophysiology is discussed in this article from New England Journal of Medicine referred to in
an earlier posting.