Abstract

Background: As shown on the basis of highly sensitive assays, cardiac troponin release is now observed after physiological heart stress and in mild heart pathologies: both considered unrelated to the irreversible cardiac alteration that is typically the source of release. Transitory cardiac membrane leakage was suggested as the basis. In our view, mild inflammation may drive this type of cardiac troponin release.
To verify this hypothesis, marathon runners who demonstrated post-run inflammation were used as a model to correlate cTnT release and inflammation intensity.
Methods: In 78 male marathon runners at three time points (pre-race, post-race, and after two weeks of rest), cardiac troponin T (cTnT) was monitored, Measurements were done with the highly sensitive assay (hs cTnT assay) and the conventional fourth-generation cTnT assay for comparison. Concurrently the inflammation markers (leukocyte and neutrophil counts, CRP, IL-6) were measured.
Results: Pre-race, the fourth-generation assay failed to demonstrate cTnT positivity (> test specific LLD). In contrast, with use of the highly sensitive assay, 28% of the participants were positive for cTnT (> LLD of hs cTnT assay).
Post-race, cTnT as measured with the fourth-generation assay was observed to be detectable in 43% of the runners (> LLD = 99th percentile cut off), but all runners had detectable cTnT values (> LLD) when measured with the highly sensitive assay. Even in 94% of these cTnT-positive runners, the value exceeded the 99th percentile cut off determined for the highly sensitive assay (13 ng/L).
cTnT release correlated significantly with inflammation intensity. Faster runners demonstrated significantly stronger cTnT releases and inflammation signs.
Conclusions: As demonstrated after physiological heart stress such as marathon running, transitory inflammation is evidently one of the events contributing to the cardiac troponin release under conditions suggested as unrelated to irreversible cardiac alteration.

DOI: Clin. Lab. 2010;56:51-58