Left Ventricle Libman-Sacks Endocarditis Secondary to Systemic Lupus Erythematosus and Antiphospholipid Syndrome: A Case Report

BACKGROUND Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by remarkable phenotypic heterogeneity. Antiphospholipid syndrome (APS) is a coagulation disorder primarily characterized by an antiphospholipid antibody-mediated prothrombotic state. Both SLE and APS can be associated with Libman-Sacks endocarditis (LSE), which may induce subendocardial inflammation followed by thrombosis and fibrosis. We report a rare case of non-valvular left-ventricular LSE in a patient with SLE/APS. These findings underscore the protean cardiac manifestations of SLE/APS-associated disease. CASE REPORT A 19-year-old woman with a 2-year history of SLE and APS presented with intermittent chest discomfort and dizziness for 4 months. Laboratory investigations revealed positive autoantibodies (antinuclear antibody, anti-dsDNA, anti-Sm, anticardiolipin IgG, anti-ß2GPI); reduced complement (C3: 42.1 mg/dL, C4: 3 mg/dL); elevated inflammatory markers (erythrocyte sedimentation rate: 96 mm/h), and mild cardiac enzyme abnormalities. Multimodal imaging demonstrated a 27×20 mm hypoechoic, non-perfused mass in the left-ventricular inferior wall on transthoracic and myocardial contrast echocardiography. Adjacent myocardium showed regional hypokinesis and wall thinning. Cardiac magnetic resonance further revealed transmural late gadolinium enhancement, confirming non-valvular LSE. Treatment included methylprednisolone, intravenous immunoglobulin, cyclophosphamide, belimumab, hydroxychloroquine, and warfarin. Six months later, the patient was clinically stable, and repeat imaging showed fibrotic transformation of the thrombus and partial recovery of regional wall motion. CONCLUSIONS This rare case of non-valvular Libman-Sacks endocarditis highlights the intricate interplay between SLE/APS and LSE. Multimodal imaging coupled with serologic testing is essential for accurate diagnosis. Long-term combined immunosuppressive and anticoagulant therapy proved effective, but further longitudinal and mechanistic studies are needed to optimize management of such rare complications.

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Publication Details

Journal
American Journal of Case Reports
Published
2025-09-16
DOI
https://doi.org/10.12659/ajcr.949826
Citations
1
Primary Topic
Blood disorders and treatments
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article
Field-Weighted Citation Impact
1.82
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Left Ventricle Libman-Sacks Endocarditis Secondary to Systemic Lupus Erythematosus and Antiphospholipid Syndrome: A Case Report

Wenqing Gong, Ying Liu, Minjuan Zheng, Zihao Yang
1 citations
American Journal of Case Reports
Blood disorders and treatments
1.82
article

Left Ventricle Libman-Sacks Endocarditis Secondary to Systemic Lupus Erythematosus and Antiphospholipid Syndrome: A Case Report

Wenqing Gong, Ying Liu, Minjuan Zheng, Zihao Yang
article en
1 citations

Abstract

BACKGROUND Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by remarkable phenotypic heterogeneity. Antiphospholipid syndrome (APS) is a coagulation disorder primarily characterized by an antiphospholipid antibody-mediated prothrombotic state. Both SLE and APS can be associated with Libman-Sacks endocarditis (LSE), which may induce subendocardial inflammation followed by thrombosis and fibrosis. We report a rare case of non-valvular left-ventricular LSE in a patient with SLE/APS. These findings underscore the protean cardiac manifestations of SLE/APS-associated disease. CASE REPORT A 19-year-old woman with a 2-year history of SLE and APS presented with intermittent chest discomfort and dizziness for 4 months. Laboratory investigations revealed positive autoantibodies (antinuclear antibody, anti-dsDNA, anti-Sm, anticardiolipin IgG, anti-ß2GPI); reduced complement (C3: 42.1 mg/dL, C4: 3 mg/dL); elevated inflammatory markers (erythrocyte sedimentation rate: 96 mm/h), and mild cardiac enzyme abnormalities. Multimodal imaging demonstrated a 27×20 mm hypoechoic, non-perfused mass in the left-ventricular inferior wall on transthoracic and myocardial contrast echocardiography. Adjacent myocardium showed regional hypokinesis and wall thinning. Cardiac magnetic resonance further revealed transmural late gadolinium enhancement, confirming non-valvular LSE. Treatment included methylprednisolone, intravenous immunoglobulin, cyclophosphamide, belimumab, hydroxychloroquine, and warfarin. Six months later, the patient was clinically stable, and repeat imaging showed fibrotic transformation of the thrombus and partial recovery of regional wall motion. CONCLUSIONS This rare case of non-valvular Libman-Sacks endocarditis highlights the intricate interplay between SLE/APS and LSE. Multimodal imaging coupled with serologic testing is essential for accurate diagnosis. Long-term combined immunosuppressive and anticoagulant therapy proved effective, but further longitudinal and mechanistic studies are needed to optimize management of such rare complications.

American Journal of Case ReportsVol. 26
Xijing Hospital (CN), Air Force Medical University (CN)
Openalex Percentile: Top 13%
Blood disorders and treatments
1.82
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