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
Conclusions-This explorative study in non-ST-segment-elevation myocardial infarction shows that cTnT is released from cardiomyocytes as a combination of cTn T-I-C complex, free intact cTnT, and multiple cTnT fragments indicating intracellular cTnT degradation. Over time, the cTn 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.
- cardiac biomarkers
- cardiac troponin T degradation
- non ST-segment elevation acute coronary syndrome
- THROMBIN ACTIVATION
- SERUM PREPARATION
- ROOT CAUSE