Dylmitr Rittoo1, Alan Jones2, Bryan Lecky3, Duncan Neithercut2. 1. Department of Cardiovascular Medicine, Wirral University Teaching Hospital, Wirral, United Kingdom. Electronic address: drittoo@nhs.net. 2. Department of Laboratory Medicine, Wirral University Teaching Hospital, Wirral, United Kingdom. 3. The Walton Centre for Neurology and Neurosurgery, Liverpool, United Kingdom.
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 cardiac troponin I (cTnI) as equally sensitive and specific for the diagnosis of myocardial injury. Although 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), creatine kinase myocardial band (CK-MB), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). RESULTS: Serial measurements (265 samples) in 25 initially hospitalized patients taken during a mean of 2.4 years showed persistent elevation of cTnT (median: 0.08 μg/l; interquartile range: 0.06 to 0.14 μg/l), CK (582 U/l; 303 to 3,662 U/l), and CK-MB (24 μg/l; 8 to 34 μg/l). In contrast, cTnI, measured using 2 sensitive assays, was persistently normal throughout the study in 22 patients. Electrocardiograms (ECGs) and echocardiograms were normal in 16 and 17 patients, respectively, and no serial changes were observed. Therapeutic interventions in patients with reversible myopathies normalized cTnT, CK, and CK-MB in unison. Single measurements in 27 ambulatory patients showed elevated CK (953 U/l; 562 to 1,320 U/l), CK-MB (18 μg/l; 11 to 28 μg/l), and cTnT (0.03 μg/l; 0.02 to 0.05 μg/l) in 21, 22, and 18 patients respectively. cTnI was abnormal in only 1 patient. NT-proBNP (41 pg/ml; 35 to 97 pg/ml) was normal in all but 2 patients. ECGs were normal in 15 patients. No patients with elevated cTnT, but with normal cTnI, had 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.
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 cardiac troponin I (cTnI) as equally sensitive and specific for the diagnosis of myocardial injury. Although 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), creatine kinase myocardial band (CK-MB), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). RESULTS: Serial measurements (265 samples) in 25 initially hospitalized patients taken during a mean of 2.4 years showed persistent elevation of cTnT (median: 0.08 μg/l; interquartile range: 0.06 to 0.14 μg/l), CK (582 U/l; 303 to 3,662 U/l), and CK-MB (24 μg/l; 8 to 34 μg/l). In contrast, cTnI, measured using 2 sensitive assays, was persistently normal throughout the study in 22 patients. Electrocardiograms (ECGs) and echocardiograms were normal in 16 and 17 patients, respectively, and no serial changes were observed. Therapeutic interventions in patients with reversible myopathies normalized cTnT, CK, and CK-MB in unison. Single measurements in 27 ambulatory patients showed elevated CK (953 U/l; 562 to 1,320 U/l), CK-MB (18 μg/l; 11 to 28 μg/l), and cTnT (0.03 μg/l; 0.02 to 0.05 μg/l) in 21, 22, and 18 patients respectively. cTnI was abnormal in only 1 patient. NT-proBNP (41 pg/ml; 35 to 97 pg/ml) was normal in all but 2 patients. ECGs were normal in 15 patients. No patients with elevated cTnT, but with normal cTnI, had 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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