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Performance of Today’s Cardiac Troponin Assays and Tomorrow’s

¹ Laboratorio Analisi Chimico Cliniche 1, Azienda Ospedaliera "Spedali Civili", 25125 Brescia, Italy, Fax 39-030-3995369, E-mail panteghi@bshosp.osp.unibs.it

International scientific bodies currently recommend the use of cardiac troponins for the detection of myocardial necrosis (1)(2). Some troponin assays, however, are inadequately appraised before their introduction in clinical use (3). The Committee on Standardization of Markers of Cardiac Damage (C-SMCD) of the IFCC proposed quality specifications for cardiac troponin assays with the objectives to help assay manufacturers and clinical laboratories and to urge the scientific community to select and design research projects on the major issues in troponin determination (4). The study by Uettwiller-Geiger et al. (5) published in this month’s issue of Clinical Chemistry represents a good example that fulfills these suggestions.

The first aspect that merits consideration is the evaluation of antibody specificity in troponin immunoassays. The issue of epitope location is important for cardiac troponin I (cTnI) assays because the amino- and carboxyl-terminal parts of the molecule are susceptible to proteolysis and this degradation may be related to the degree of tissue ischemia (6). Intact cTnI and up to 11 modified products have been detected in the sera of patients with acute myocardial infarction (MI) (6). cTnI is released predominately as a binary complexed form with troponin C (IC), although a minor amount of free cTnI is also found in the bloodstream (7). Moreover, cTnI is released in both oxidized and reduced forms, the oxidation being the result of intramolecular disulfide formation by two cysteine residues (8). Finally, cTnI can also be phosphorylated (8).

Studies of clinical troponin assays must examine the specificities of antibody pairs used in the assays. Preferably the antibodies should . . . [Full Text of this Article]

Acknowledgments

References

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