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Libman-Sacks endocarditis and embolic cerebrovascular disease
Carlos A Roldan1, Wilmer L Sibbitt, Clifford R Qualls
1Division of Cardiology, University of New Mexico School of Medicine and New Mexico VA Health Care Center, Albuquerque, New Mexico.
JACC. Cardiovascular Imaging
|September 14, 2013
Summary
Libman-Sacks endocarditis significantly increases the risk of cerebrovascular disease (CVD) in patients with systemic lupus erythematosus (SLE). This condition is a likely source of cerebral emboli, leading to neurocognitive dysfunction and brain lesions.
Area of Science:
- Cardiology
- Neurology
- Rheumatology
Background:
- The cardioembolic pathogenesis of cerebrovascular disease (CVD) in neuropsychiatric systemic lupus erythematosus (NPSLE) remains incompletely understood.
- Established links between Libman-Sacks endocarditis and CVD in SLE are lacking.
- This study investigates the role of Libman-Sacks endocarditis in SLE-related CVD.
Purpose of the Study:
- To determine if Libman-Sacks endocarditis is a pathogenic factor for cerebrovascular disease (CVD) in systemic lupus erythematosus (SLE).
- To assess the association between Libman-Sacks endocarditis and various manifestations of CVD in SLE patients.
- To evaluate the impact of Libman-Sacks endocarditis on neurocognitive function and brain lesions in SLE.
Main Methods:
- A 6-year prospective study involving 30 patients with acute NPSLE, 46 SLE controls, and 26 healthy controls.
- Comprehensive evaluations included transesophageal echocardiography, Doppler ultrasound, neurocognitive testing, and brain MRI/MRA.
- Clinical follow-up was conducted for a median of 52 months.
Main Results:
- Libman-Sacks vegetations were significantly more prevalent in NPSLE patients (87%) compared to SLE (28%) and healthy controls (8%).
- Patients with vegetations exhibited higher rates of cerebromicroembolism, neurocognitive dysfunction, and cerebral infarcts.
- Libman-Sacks vegetations were identified as independent risk factors for NPSLE, neurocognitive dysfunction, and brain lesions.
Conclusions:
- Libman-Sacks endocarditis is associated with an elevated risk of embolic CVD in SLE patients.
- The findings suggest that Libman-Sacks endocarditis serves as a significant source of cerebral emboli in the context of SLE.
- Therapeutic interventions targeting Libman-Sacks endocarditis may mitigate CVD risk in SLE.
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