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Historical troponin I development addressed CK-MB specificity gaps; leaves open refinement of modern high-sensitivity assays in practice.
Featured Article: Adams JE III, Bodor GS, Davila-Roman VG, Delmez JA, Apple FS, Ladenson JH, Jaffe AS. Cardiac troponin I: a marker with high specificity for cardiac injury. Circulation 1993;88:101–6.2 By the late 1980s, it was clear that there were frequent increases of creatine kinase-muscle–brain (CK-MB)3 in patients with renal failure, hypothyroidism, pulmonary embolism, and a variety of skeletal muscle pathologies. Thus, there were often questions about whether such increases were due to the release from tissues other than the heart and especially from skeletal muscle where there is reexpression of B-chain CK protein in response to injury. These questions made the triage of patients with increased CK-MB values difficult, especially when conjoint skeletal muscle and cardiac muscle injury was present as is common postoperatively (1). Because of these difficulties, there was interest in developing more clinically specific cardiac markers. Initially, cardiac troponin T (cTnT) was introduced, but there were questions related to its clinical specificity. These questions subsequently were found to result from antibody cross-reactivity with skeletal muscle troponin, and that problem was …
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Allan S. Jaffe (2017) studied this question.
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