Multi-Site Coronary Vein Sampling Study on Cardiac Troponin T Degradation in Non–ST-Segment–Elevation Myocardial Infarction: Toward a More Specific Cardiac Troponin T Assay

Sander A. J. Damen, Wim H. M. Vroemen, Marc A. Brouwer, Stephanie T. P. Mezger, Harry Suryapranata, Niels van Royen, Otto Bekers, Steven J. R. Meex, Will K. W. H. Wodzig, Freek W. A. Verheugt, Douwe de Boer, G. Etienne Cramer, Alma M. A. Mingels

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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 cTn T-I-C complex, free intact cTnT, and 29 kDa and 15 to 18 kDa cTnT fragments, all in higher concentrations than in simultaneously obtained peripheral samples. While cTn T-I-C complex proportionally decreased, and disappeared over time, 15 to 18 kDa cTnT fragments increased. Moreover, cTn 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 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.
Original languageEnglish
Article numbere012602
JournalJournal of the American Heart Association
Issue number14
Publication statusPublished - 1 Jan 2019
Externally publishedYes

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