Author: Rittoo D, Jones A, Lecky B, Neithercut D
Abstract: OBJECTIVES: This study sought to determine the clinical and biological significance of elevated cardiac Troponin T (cTnT) in patients with neuromuscular diseases.
BACKGROUND: Practice guidelines regard cTnT and cTnI as equally sensitive and specific for the diagnosis of myocardial injury. Whereas cTnI is unique to myocardium cTnT can be re-expressed in skeletal muscle in response to injury. The commercial cTnT assay is claimed to be cardiac specific.
METHODS: Fifty two patients with 20 different types of acquired and inherited neuromuscular diseases underwent full clinical assessment, cardiac investigations and measurements of serum cTnT , cTnI , creatine kinase (CK), CK-MB and N-terminal pro B-type natriuretic peptide (NT-proBNP) .
RESULTS: Serial measurements (265 samples) in 25 initially hospitalised patients over a mean of 2.4 years, showed persistent elevation of cTnT ( median: 0.08; interquartile range: 0.06 - 0.14 μg/L) , CK (582; 303- 3662 U/L) and CK-MB ( 24; 8 - 34 μg/L). In contrast cTnI, measured using 2 sensitive assays, was persistently normal throughout in 22 patients. Electrocardiograms and echocardiograms were normal in 16 and 17 patients respectively and no serial changes were observed. Therapeutic interventions in patients with reversible myopathies normalised cTnT, CK and CK-MB in unison. Single measurements in 27 ambulatory patients showed elevated CK (953; 562-1320 U/L), CK-MB (18;11-28 μg/L) and cTnT (0.03; 0.02 - 0.05 μg/L), in 21, 22 and 18 patients respectively. cTnI was abnormal in only 1 patient. NT-proBNP (41; 35- 97 pg/mL ) was normal in all but 2 patients. ECG was normal in 15 patients. No patients with elevated cTnT but normal cTnI sustained any cardiovascular events in either group during follow up.
CONCLUSIONS: Patients with a wide spectrum of neuromuscular diseases commonly have persistent elevation of cTnT and CK-MB in the absence of clinical and cTnI evidence of myocardial injury. Re-expressed cTnT in diseased skeletal muscle appears to be the source of the elevated cTnT detected in the circulation of these patients.
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