Cardiac troponin T release and inflammation demonstrated in marathon runners
Silvia Gilka Munzoz Saravia1, Fabian Knebel, Sabrina Schroeckh
1Medizinische Klinik (Kardiologie), Charité--Universitätsmedizin Berlin, Berlin, Germany.
Insights
Mild inflammation can cause cardiac troponin T (cTnT) release after marathon running, even without permanent heart damage. This study links inflammation intensity to cTnT levels in runners, suggesting inflammation as a key factor.
Area of Science:
- Cardiology
- Exercise Physiology
- Biomarkers
Background:
- Cardiac troponin T (cTnT) release is observed after physiological stress and mild heart conditions, previously thought unrelated to irreversible cardiac damage.
- Transitory cardiac membrane leakage was hypothesized, but mild inflammation is proposed as a potential driver for cTnT release.
Purpose of the Study:
- To investigate the hypothesis that mild inflammation drives cardiac troponin T release.
- To correlate cardiac troponin T release intensity with inflammation markers in marathon runners.
Main Methods:
- 78 male marathon runners were monitored for cardiac troponin T (cTnT) using both highly sensitive (hs cTnT) and conventional assays at pre-race, post-race, and post-rest time points.
- Inflammation markers including leukocyte and neutrophil counts, CRP, and IL-6 were measured concurrently.
- Comparison between hs cTnT assay and conventional assay for cTnT detection was performed.
Main Results:
- The highly sensitive assay detected cTnT in 28% of runners pre-race, while the conventional assay did not.
- Post-race, all runners showed detectable cTnT with the hs cTnT assay, with 94% exceeding the 99th percentile cutoff.
- cTnT release significantly correlated with inflammation intensity; faster runners exhibited stronger cTnT release and inflammation.
Conclusions:
- Transitory inflammation is a contributing factor to cardiac troponin T release following physiological stress, such as marathon running.
- This finding supports that cTnT release can occur without irreversible cardiac alteration, driven by inflammatory processes.
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 are [corrected] 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 who participated in the BERLIN-MARATHON 2006, cardiac troponin T (cTnT) was monitored [corrected] at three time points (pre-race, post-race, and after two weeks of rest). [corrected] Measurements were done with the highly sensitive assay (hs cTnT assay) and the conventional fourth-generation cTnT assay for comparison. Concurrently, [corrected] 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 the [corrected] 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 = 99(th) 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 99(th) 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.
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