Case report: Systemic lupus erythematosus combined with myocardial hypertrophy

Author:

Wang Shanshan12ORCID,Wei Xinfeng2,Yang Wenqing13,Zhang Dan45

Affiliation:

1. Innovative Institute of Chinese Medicine and Pharmacy Shandong University of Traditional Chinese Medicine Jinan China

2. The Fifth People's Hospital of Jinan Jinan China

3. Shandong Engineering Laboratory of Traditional Chinese Medicine Precise Therapy for Cardiovascular Diseases Jinan China

4. Experimental Center Shandong University of Traditional Chinese Medicine Jinan China

5. Key Laboratory of Traditional Chinese Medicine Classical Theory, Ministry of Education Shandong University of Traditional Chinese Medicine Jinan China

Abstract

AbstractObjectiveSystemic lupus erythematosus (SLE) is a multisystem‐involved, highly heterogeneous autoimmune disease with diverse clinical manifestations. We report an extremely rare case of SLE with severe diffuse myocardial hypertrophy.MethodsThe patientʼs echocardiography and cardiac magnetic resonance imaging (CMR) results indicated diffuse myocardial hypertrophy. After excluding coronary atherosclerosis, hypertensive cardiomyopathy, drug toxicity, and other causes, the patient was diagnosed with SLE‐specific cardiomyopathy. Medications such as hormones, antimalarials, immunosuppressants, and biologics were administered.ResultsAncillary test results were as follows: hs‐cTnI: 0.054 ng/mL (0–0.016); NTproBNP: 1594.0 pg/mL (<150); A contrast‐enhanced CMR revealed the diffuse thickening of the left ventricular wall with multiple abnormal enhancements, reduced left ventricular systolic and diastolic function, and moderate amount of pericardial effusion. Endomyocardial myocardial biopsy was performed, showing cardiomyocyte hypertrophy and degeneration, and no changes in myocarditis or amyloidosis. The pathology viewed by electron microscopy showed increased intracellular glycogen in the myocardium, and no hydroxychloroquine‐associated damage in the myocardium. The 24‐h ambulatory blood pressure and contrast‐enhanced computed tomography of coronary arteries were normal. The diagnosis of SLE‐specific cardiomyopathy was clear. The myocardial hypertrophy showed reversible alleviation following treatment with high‐dose corticosteroids. CMR results before and after treatment were as follows: interventricular septum, pretreatment (28) versus post‐treatment (22) mm; left ventricular inferior wall, pretreatment (18–21) versus post‐treatment (12–14) mm; left ventricular lateral wall, pretreatment (17–18) versus post‐treatment (10–12) mm; pericardial effusion (left ventricular lateral wall), pretreatment (25) versus post‐treatment (12) mm; left ventricular ejection fraction, pretreatment (38.9%) versus post‐treatment (66%).ConclusionMyocardial hypertrophy may be an important sign of active and prognostic assessment in SLE diagnosis and management. Similarly, when encountering cases of myocardial hypertrophy, the possibility of autoimmune disease should be considered in addition to common causes.

Publisher

Wiley

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