Key result
Coronary venous high-sensitivity cTnT is ~28% higher than peripheral levels, revealing complex fragment release.
Why the study?
Cardiac troponin T is present in conditions other than myocardial infarction, with distinct forms whose in vivo formation is incompletely understood.
What is the composition and degradation pattern of cardiac troponin T released during NSTEMI?
Observational (n=71)
What is the composition and degradation pattern of cardiac troponin T released during NSTEMI?
Effect estimate: 28% higher
p-value: p=<0.001
cTnT is released from cardiomyocytes as a combination of complexes and fragments that degrade over time, suggesting potential for developing more specific cTnT assays for myocardial infarction.
May inform more specific cTnT assay development for NSTEMI; leaves open clinical impact pending prospective validation.
Background Cardiac troponin T ( cTnT ) is seen in many other conditions besides myocardial infarction, and recent studies demonstrated distinct forms of cTnT . At present, the in vivo formation of these different cTnT forms is incompletely understood. We therefore performed a study on the composition of cTnT during the course of myocardial infarction, including coronary venous system sampling, close to its site of release. Methods and Results Baseline samples were obtained from multiple coronary venous system locations, and a peripheral artery and vein in 71 non– ST ‐segment–elevation myocardial infarction patients. Additionally, peripheral blood was drawn at 6‐ and 12‐hours postcatheterization. cTnT concentrations were measured using the high‐sensitivity‐ cTnT immunoassay. The cTnT composition was determined via gel filtration chromatography and Western blotting in an early and late presenting patient. High‐sensitivity ‐ cTnT concentrations were 28% higher in the coronary venous system than peripherally (n=71, P <0.001). Coronary venous system samples demonstrated cT n T‐I‐C complex, free intact cTnT , and 29 kD a and 15 to 18 kD a cTnT fragments, all in higher concentrations than in simultaneously obtained peripheral samples. While cT n T‐I‐C complex proportionally decreased, and disappeared over time, 15 to 18 kD a cTnT fragments increased. Moreover, cT n T‐I‐C complex was more prominent in the early than in the late presenting patient. Conclusions This explorative study in non– ST ‐segment–elevation myocardial infarction shows that cTnT is released from cardiomyocytes as a combination of cT n T‐I‐C complex, free intact cTnT , and multiple cTnT fragments indicating intracellular cTnT degradation. Over time, the cT n T‐I‐C complex disappeared because of in vivo degradation. These insights might serve as a stepping stone toward a high‐sensitivity‐ cTnT immunoassay more specific for myocardial infarction.
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Damen et al. (2019) conducted an observational in Non-ST-segment-elevation myocardial infarction (n=71). Coronary venous system sampling vs. Peripheral artery and vein sampling was evaluated on High-sensitivity cTnT concentrations (28% higher, p=<0.001). High-sensitivity cTnT concentrations were 28% higher in the coronary venous system than peripherally (P<0.001), revealing release as a complex, free intact cTnT, and multiple fragments.
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