Original Article

Clinical Rheumatology

, Volume 29, Issue 10, pp 1107-1111

Clinical observations on the significance of raised cardiac troponin-T in patients with myositis of varying etiologies seen in rheumatology practice

  • Corinne FisherAffiliated withDepartment of Rheumatology, Southend University Hospital, NHS Trust
  • , Sumeet AgrawalAffiliated withDepartment of Rheumatology, Southend University Hospital, NHS Trust
  • , Way Main WongAffiliated withDepartment of Rheumatology, Southend University Hospital, NHS Trust
  • , Mike Fahie-WilsonAffiliated withDepartment of Clinical Biochemistry, Southend University Hospital
  • , Bhaskar DasguptaAffiliated withDepartment of Rheumatology, Southend University Hospital, NHS Trust Email author 

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To study the source and clinical relevance of elevated cardiac troponin-T (cTnT) in patients with inflammatory myositis of varying etiology is the objective of this study. Patients with new-onset myositis of varying etiologies and raised serum cTnT and creatine kinase (CK) were identified. Clinical myocardial disease was ruled out on the basis of history, examination, ECG, and 2D-echocardiography. Along with serial estimation of CK levels, cTnT isoforms specific to myocardium (by electrochemiluminescence immunoassay) were used for serial estimation of cTnT levels. Gel-filtration chromatography was performed to investigate the nature of elevated cTnT in myositis patients compared to that in acute coronary syndrome (ACS). Patients requiring hospitalization due to an indication related to myositis were classified as having severe disease. All patients received conventional management for myositis as indicated in individual cases. Eleven patients (eight women, three men; aged 59–87 years) with polymyositis (five), dermatomyositis (three), statin-induced myopathy (two), and inclusion body myositis (one) were studied. The cTnT in myositis patients was found to be identical to cTnT in ACS. The time kinetics of cTnT was different from CK and their levels did not correlate. While CK normalized with treatment, cTnT levels exhibited prolonged elevation. Nine of the patients with raised cTnT had severe disease despite absence of clinical myocardial disease. Three died. cTnT in sera of patients with inflammatory muscle disease is of cardiac origin. It may identify a subgroup with subclinical myocardial involvement with differential response to treatment compared to skeletal muscle. We feel cTnT is an important laboratory investigation in patients with myositis.


Cardiac troponin Dermatomyositis Muscle Myositis Polymyositis Statin-induced myositis