Troponin Release Mechanisms and Circulating Forms: Toward Injury-Specific Immunoassays
Different etiologies of myocardial injury produce distinct circulating forms of cardiac troponin I and T, arising from varied release mechanisms including necrosis, apoptosis, and membrane blebbing. This review synthesizes evidence on how characterizing these molecular forms across clinical settings could inform the development of immunoassays capable of distinguishing injury types. Such differentiation could potentially address the reduced clinical specificity of current high-sensitivity assays, which detect troponin elevations across a broad range of cardiac and non-cardiac conditions.
The original study
Myocardial Injury and the Release of Troponins I and T in the Blood of Patients.
- Authors
- Katrukha IA, Katrukha AG
- Journal
- Clinical chemistry
- Type
- Journal Article, Review
- PMID
- 33418589
Original abstract
BACKGROUND: Cardiac troponin I (cTnI) and cTnT are the established biomarkers of cardiomyocyte damage and the recommended biomarkers for the diagnosis of acute myocardial infarction (MI). High-sensitivity immunochemical diagnostic systems are able to measure the cTn concentrations in the blood of a majority of healthy people. At the same time, the concentration of cTn may be increased not only after MI but also because of other pathologies that might affect myocardium. This effect reduces the clinical specificity of cTn for MI and may complicate the diagnosis. CONTENT: This review summarizes the existing information regarding the causes and mechanisms that lead to the increase of cTn concentration in blood and the forms of cTn that are present in circulation after MI or other types of myocardial injury. SUMMARY: Different etiologies of disease associated with increases of cTn above the 99th percentile and various mechanisms of troponin release from myocardium could result in the appearance of different forms of cTn in blood and provide the first clinical evidence of injury. Additional research is needed for the careful characterization of cTn forms that are present in the blood in different clinical settings. That knowledge may lead to the development of immunochemical systems that would differentiate certain forms of troponins and possibly certain types of cardiac disease.