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.
Background
Cardiac troponin I and T are both used for diagnosing myocardial infarction (MI) after coronary artery bypass grafting (CABG), also known as type 5 MI (MI-5). Different MI-5 definitions have been formulated, using multiples of the 99th percentile upper reference limit (10×, 35×, or 70× URL), with or without supporting evidence. These definitions are arbitrarily chosen based on conventional assays and do not differentiate between troponin I and T. We therefore investigated the kinetics of high-sensitivity cardiac troponin I (hs-cTnI) and T (hs-cTnT) following CABG.
Methods
A systematic search was applied to MEDLINE and EMBASE databases including the search terms “coronary artery bypass grafting” AND “high-sensitivity cardiac troponin.” Studies reporting hs-cTnI or hs-cTnT on at least 2 different time points were included. Troponin concentrations were extracted and normalized to the assay-specific URL.
Results
For hs-cTnI and hs-cTnT, 17 (n = 1661 patients) and 15 studies (n = 2646 patients) were included, respectively. Preoperative hs-cTnI was 6.1× URL (95% confidence intervals: 4.9–7.2) and hs-cTnT 1.2× URL (0.9–1.4). Mean peak was reached 6–8 h postoperatively (126× URL, 99–153 and 45× URL, 29–61, respectively). Subanalysis of hs-cTnI illustrated assay-specific peak heights and kinetics, while subanalysis of surgical strategies revealed 3-fold higher hs-cTnI than hs-cTnT for on-pump CABG and 5-fold for off-pump CABG.
Conclusion
Postoperative hs-cTnI and hs-cTnT following CABG surpass most current diagnostic cutoff values. hs-cTnI was almost 3-fold higher than hs-cTnT, and appeared to be highly dependent on the assay used and surgical strategy. There is a need for assay-specific hs-cTnI and hs-cTnT cutoff values for accurate, timely identification of MI-5.
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