Elevated Cardiac Troponin T in Patients with Lupus Myositis Presenting with Noncardiac Chest Pain
Guy Katz1, Sharon L Kolasinski2, Baskaran Sundaram3
1Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Bulfinch 165, 55 Fruit St., Boston, MA 02114, USA.
Insights
Systemic lupus erythematosus (SLE) myositis can elevate cardiac troponin T (cTnT), mimicking heart attack. Elevated cTnT in SLE myositis may indicate skeletal muscle damage, not cardiac injury, necessitating careful interpretation of cardiac biomarkers.
Area of Science:
- Rheumatology
- Cardiology
- Clinical Diagnostics
Background:
- Systemic lupus erythematosus (SLE) patients presenting with chest pain face diagnostic challenges.
- Cardiac troponin T and I (cTnT, cTnI) are key biomarkers for myocardial injury.
- Elevated cTnT in idiopathic inflammatory myopathies reflects skeletal muscle breakdown, not cardiac damage.
Abstract:
Patients with systemic lupus erythematosus (SLE) presenting with chest pain pose a unique diagnostic challenge, with causes ranging from cardiopulmonary disease to esophageal disorders and musculoskeletal chest wall pain. The most common biomarkers for myocardial injury are cardiac troponin T and I (cTnT and cTnI) due to their high sensitivity for the early detection of myocardial infarction. In the idiopathic inflammatory myopathies, cTnT is commonly elevated, and this reflects skeletal muscle breakdown rather than myocardial damage. Similar observations have not been reported in SLE myositis to date. We present two cases of patients with SLE and associated myositis who presented with chest pain and elevated cTnT. Both patients had a normal cTnI, transthoracic echocardiogram, and cardiac magnetic resonance imaging, likely indicating noncardiac chest pain. Clinicians should be aware that the specificity of cTnT might be lower in SLE myositis and that cTnI elevation may be more specific in detecting myocardial insult.
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