• Cardiogenic shock
• Lupus myocarditis
• Systemic lupus erythematosus

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.

Fulminant lupus myocarditis is a rare but fatal manifestation of systemic lupus erythematosus. Aggressive immunosuppressive treatments are important in its successful management. However, they can significantly damage the immunity and are associated with a considerable risk of infection development and spread. We present a rare and complicated case of a 20-year-old female diagnosed with fulminant lupus myocarditis accompanied by pneumonia. The patient was successfully treated with plasma exchange (PE) for fulminant lupus myocarditis.

A 20-year-old Chinese woman presented to the Hematology Department complaining of fatigue and knee pain. Blood test showed anemia and thrombocytopenia. On the second day of hospitalization, she was transferred to the ICU due to dyspnea and hypotension. Autoimmune profiles showed hypocomplementemia and positive antinuclear antibodies. Computer tomography showed an enlarged heart and pneumonia. Ultrasound revealed an enlarged heart with a low left ventricular ejection fraction. Fulminant lupus myocarditis with cardiogenic shock was initially considered. Due to the accompanying pneumonia, aggressive immunosuppression was contraindicated. Her cardiac function remained critical after the initial therapy of intravenous immunoglobulin and corticosteroids at a conventional dose, but she responded well to later PE therapy plus corticosteroids administration. The patient fully recovered with normal cardiac function.

This case indicates that PE is a valuable treatment choice without adverse effects of immunosuppression in patients with fulminant lupus myocarditis and coexisting infection.

• Plasma exchange
• Cardiogenic shock
• Lupus myocarditis
• Systemic lupus erythematosus
• Immunosuppressive treatment
• Case report