Cardiac troponin complexes and fragments: potential targets for improved clinical performance

High-sensitivity assays for cardiac troponin (cTn) have improved rule-out algorithms for acute myocardial infarction (AMI). However, reduced specificity specifically to AMI posed new clinical challenges. Studies involving the composition of troponin released into the circulation after injury may provide insights to improve specificity. In MI patients, cTnI primarily exists of cTnIC and truncated cTnTIC complexes. Larger-sized cTnT forms, as part of the cTnTIC complex, predominate with shorter ischemic time windows. Over time, mildly and heavily truncated cTnT forms increase, whereas for cTnI this is less certain. Targeting the central part of cTnT, the current high-sensitivity assay also identifies heavily truncated forms as seen in end-stage renal disease and after exercise. This review on composition of circulating troponin covers different populations and outlines first initiatives toward more specific assays by targeting larger-sized troponin forms.