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To T or not to T, that is the question.

The quest for a test that is absolutely disease- and tissue-specific could be considered the Holy Grail of the clinical chemist, dreamt of but seldom achieved. Initial reports on measurement of the cardiac troponins, cardiac troponin T (cTnT) and cardiac troponin I (cTnI), for diagnosis of myocardial infarction suggested that these markers would become the “gold standard,” replacing all other existing tests. Questions have been raised as to the specificity of cTnT for cardiac damage in patients with extreme rhabdomyolysis, renal failure, polymyositis, and muscular dystrophy. This problem is addressed by the papers of Bodor et al. (1) and Muller-Bardorff et al. (2) in this issue of Clinical Chemistry . This is therefore a reasonable time to review what we know at the basic science level and how this relates to both papers and current clinical practice.

Cardiac and skeletal muscle cells are closely related but arise from different embryonic lineages and express distinctive gene sets when terminally differentiated. During embryonic development, both muscle types cross-express several genes. There are three troponin T genes, corresponding to slow skeletal, fast skeletal, and cardiac troponin. During early embryonic development, the cTnT gene is activated and transcribed at relatively low levels in both cardiac and skeletal muscles until mid-fetal development, when expression is divergently regulated. In cardiac cells, transcription of the cTnT gene is sharply up-regulated, whereas in the skeletal cells it is repressed (3)(4)(5). Similarly, three isoforms of troponin I exist, also the products of three separate genes: fast skeletal muscle, slow skeletal muscle, and cardiac muscle troponin I. During fetal development, slow skeletal muscle troponin I is the predominant isoform in the heart. After birth, the slow skeletal isoform is lost such that, by 9 months of postnatal development, the cardiac isoform is the only detectable isoform …