Diseased Skeletal Muscle: A Noncardiac Source of Increased Circulating Concentrations of Cardiac Troponin T
What is the expression of immunoreactive cardiac troponin T (cTnT) expression in diseased skeletal muscle leading to possible false-positive increases in cTnT?
Patients with myopathies seen in the Neuromuscular Clinic at the Mayo Clinic were screened for increases in cTnT. If present, an assay for cTnI was performed. If normal, skeletal biopsy tissue was obtained for Western blot analysis using the capture and detection antibodies from both the fourth-generation and high-sensitivity cTnT assays. Results were compared with findings in normal cardiac tissue.
Sixteen patients had increases in cTnT, but not cTnI. All had a myopathy by clinical evaluation, clinical testing, and biopsy. Four residual biopsy samples were obtained. All three antibodies used in the cTnT (M11.7, M7) and high-sensitivity cTnT (5D8, M7) assays were immunoreactive with a 37- to 39-kDa protein in all four diseased skeletal muscle biopsy specimens and in cardiac tissue. A second immunoreactive isoform (34 to 36 kDa) was also found in one patient. None of the noncardiac control tissues expressed immunoreactive protein.
The authors concluded that there are troponin isoforms in diseased skeletal muscle that could cause increases in circulating levels of cTnT.
This study suggests that increased concentrations of cTnT detected in patients with skeletal muscle disease could be derived from diseased skeletal muscle. Clinicians need to be aware of this fact when evaluating patients for potential cardiovascular disease who may have an underlying skeletal myopathy, especially in individuals with atypical clinical presentations and isolated increases of cTnT without supportive clinical findings.
Keywords: Cytoskeletal Proteins, Biological Markers, Protein Isoforms, Biopsy, Cardiovascular Diseases, Troponin T, Muscular Diseases
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