Key result
High-sensitivity troponin assays reveal non-necrotic release mechanisms expanding biomarker utility across various conditions.
Why the study?
High-sensitivity assays detect cardiac troponins in diverse clinical conditions and healthy individuals, suggesting release mechanisms beyond cardiac necrosis that warrant discussion.
This review highlights that cardiac troponins can be released through mechanisms independent of cell necrosis, expanding their utility as biomarkers in various clinical conditions and healthy subjects.
The cardiac troponins (cTns), cardiac troponin C (cTnC), cTnT, and cTnI are key elements of myocardial apparatus, fixed as protein complex on the thin filament of sarcomere and are involved in the regulation of excitation–contraction coupling of cardiomyocytes in the presence of Ca 2+ . Circulating cTnT and cTnI (cTns) increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction (AMI). However, the use of high sensitivity (hs)‐immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can be measured also in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis. In this review, the molecular/cellular mechanisms involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events, in addition to cardiac necrosis, are discussed.
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Ragusa et al. (2022) conducted a review in Acute myocardial infarction and other clinical conditions. High-sensitivity immunoassay for cTnT and cTnI was evaluated. High-sensitivity immunoassays for cardiac troponins (cTnI and cTnT) reveal mechanisms of release independent of cardiac cell necrosis, expanding their utility as biomarkers for various conditions.
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