ArticleThe American journal of case reports2025
Left Ventricle Libman-Sacks Endocarditis Secondary to Systemic Lupus Erythematosus and Antiphospholipid Syndrome: A Case Report.
Article in The American journal of case reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Severe Mitral Regurgitation and Constrictive Pericarditis in a Patient with Systemic Lupus Erythematosus.CASE (Philadelphia, Pa.) · 2026Article
- Cardiovascular Involvement in Systemic Lupus Erythematosus: Focus on Arrhythmias.Diagnostics (Basel, Switzerland) · 2026Review
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4 authors.
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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.
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