# Rapidly progressive mitral valve disease from non-bacterial thrombotic endocarditis to mitral stenosis in systemic lupus erythematosus: a case report

**Authors:** Saaya Ichikawa-Ogura, Yasuhide Mochizuki, Eiji Toyosaki, Hiroto Fukuoka, Toshiro Shinke

PMC · DOI: 10.1093/ehjcr/ytaf098 · European Heart Journal. Case Reports · 2025-02-25

## TL;DR

A rare case shows how heart valve disease in a lupus patient progressed from one type of valve issue to another, resembling rheumatic heart disease.

## Contribution

This case report highlights an unusual progression of non-bacterial thrombotic endocarditis to mitral stenosis in a patient with SLE and APS.

## Key findings

- Non-bacterial thrombotic endocarditis initially caused mitral regurgitation, which improved with vitamin K antagonist therapy.
- The patient later developed rheumatic-like mitral stenosis requiring surgical valve replacement.
- The patient suffered a fatal cerebral infarction post-surgery, likely due to antiphospholipid syndrome.

## Abstract

Libman–Sacks endocarditis), a non-bacterial thrombotic endocarditis (NBTE) linked to systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), typically causes valve regurgitation and embolism but can rarely mimic rheumatic mitral stenosis (MS).

This case involves a 59-year-old woman with a history of APS and SLE who presented with worsening dyspnoea and congestive heart failure. Initially, severe mitral regurgitation (MR) due to NBTE resolved with vitamin K antagonist therapy, yet she subsequently developed significant MS with commissural fusion, a rheumatic-like feature. Despite stable SLE activity, echocardiography revealed severe MS with high pulmonary pressures, warranting surgical valve replacement. Intraoperative findings confirmed rheumatic-like degeneration, but the patient experienced a fatal cerebral infarction post-surgery, likely due to APS.

This case highlights the progression of NBTE-related MR to rheumatic-like MS in an SLE patient with APS, an unusual clinical course. It underscores the importance of echocardiographic monitoring in similar cases, as chronic inflammatory changes in APS might mimic rheumatic pathology, necessitating vigilant management and timely intervention.

## Linked entities

- **Diseases:** systemic lupus erythematosus (MONDO:0007915), antiphospholipid syndrome (MONDO:0017278), Libman–Sacks endocarditis (MONDO:0850223), non-bacterial thrombotic endocarditis (MONDO:0000610), mitral stenosis (MONDO:0005852), rheumatic heart disease (MONDO:0006955), congestive heart failure (MONDO:0005009), cerebral infarction (MONDO:0002679)

## Full-text entities

- **Diseases:** MS (MESH:D008946), cerebral infarction (MESH:D002544), Libman-Sacks endocarditis (MESH:D008180), NBTE (MESH:D059905), rheumatic (MESH:D012216), APS (MESH:D016736), embolism (MESH:D004617), valve regurgitation (MESH:D006349), inflammatory (MESH:D007249), MR (MESH:D008944), congestive heart failure (MESH:D006333)
- **Chemicals:** vitamin K antagonist (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11886785/full.md

## References

14 references — full list in the complete paper: https://tomesphere.com/paper/PMC11886785/full.md

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Source: https://tomesphere.com/paper/PMC11886785