Open AccessMulti‐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
Author(s) -
Damen Sander A. J.,
Vroemen Wim H. M.,
Brouwer Marc A.,
Mezger Stephanie T. P.,
Suryapranata Harry,
Royen Niels,
Bekers Otto,
Meex Steven J. R.,
Wodzig Will K. W. H.,
Verheugt Freek W. A.,
Boer Douwe,
Cramer G. Etienne,
Mingels Alma M. A.
Publication year - 2019
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.119.012602
Subject(s) - medicine , troponin complex , myocardial infarction , cardiology , troponin t , troponin , venous blood
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.