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Systemic Lupus Erythematosus Complicated with Hypertrophic Cardiomyopathy: A Case Report and Literature Review
Huihui Ma1,2, Xin Cao3, Jing Zhang1,2
1Department of Cardiology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan 610072, China.
Insights
Systemic lupus erythematosus patients on immunosuppressants may develop hypertrophic cardiomyopathy (HCM). This case highlights secondary HCM possibly linked to tacrolimus, emphasizing the need for cardiac monitoring in SLE patients.
Area of Science:
- Cardiology
- Rheumatology
- Pharmacology
Background:
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease.
- Long-term immunosuppressive therapy is common in SLE management.
- Hypertrophic cardiomyopathy (HCM) is a complex cardiac condition.
Observation:
- A 32-year-old female with a 7-year history of SLE presented with a one-year history of hypertrophic cardiomyopathy (HCM).
- The patient was on long-term treatment with cyclophosphamide, cyclosporine, methotrexate, and tacrolimus.
- Echocardiography and cardiac magnetic resonance (CMR) revealed significant left ventricular (LV) thickening (21 mm).
Findings:
- Genetic testing did not reveal pathogenic variations for HCM.
- No significant enhancement was observed in CMR, suggesting secondary HCM.
- The HCM was clinically diagnosed as secondary to SLE or tacrolimus use.
Implications:
- This case underscores the potential for iatrogenic cardiomyopathy in SLE patients undergoing immunosuppressive therapy.
- Regular cardiac monitoring, including echocardiography and CMR, is crucial for early detection of cardiac complications in SLE.
- Further research is needed to elucidate the specific mechanisms linking tacrolimus and HCM in SLE patients.
Abstract:
A 32-year-old female with systemic lupus erythematosus (SLE) for more than 7 years, and long-term treatment with cyclophosphamide, cyclosporine, methotrexate, and tacrolimus, later found to be combined with hypertrophic cardiomyopathy (HCM) for one year. The patient denied a family history of cardiomyopathy and sudden cardiac death (SCD). Echocardiography suggested that uneven thickening of the left ventricle (LV), mainly in the lower middle segment. Cardiac magnetic resonance (CMR) showed that the walls of the left ventricular (LV) were significantly thickened, as about 21 mm, mainly in the middle and lower segments. Genetic tests showed no known or suspected pathogenic variations were found and no significant enhancement in CMR, so secondary HCM was diagnosed clinically. After symptomatic treatment, the patient was discharged, and long-term follow-up was conducted. The diagnosis of HCM, which combined with SLE or second to usage of tacrolimus, was based on symptoms, echocardiography, and CMR; no endomyocardial biopsies were performed.
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