Clinical and Analytical Standardization Issues Confronting Cardiac Troponin I

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Abstract
Troponin I, a subunit of the ternary troponin complex, is a regulatory protein of the thin filament of striated muscle. Cardiac troponin I (cTnI) is uniquely different from the troponin I found in either slow or fast skeletal muscle. Possessing an additional 31-amino acid sequence at its N terminus, cTnI is found exclusively in the myocardium and, therefore, has been extensively studied as a sensitive and specific serum marker for myocardial injury (1). The forms of cTnI found in the circulation include complexes with troponin T and C (TIC and IC) as well as free subunits (2). In addition, cTnI has been identified in oxidized, reduced, and phosphorylated forms (3)(4). The signals generated by immunoassays developed with anti-cTnI monoclonal antibodies are dependent on the epitope region recognized by these antibodies (5). Thus, protein regions within the cTnI molecule that are susceptible to oxidation, reduction, or phosphorylation or to degradation by the action of proteases are likely to exhibit variable immunoreactivity and even loss of reactivity, leading to altered signal generation in cTnI immunoassays that use antibodies against such regions.