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Medline ® Abstract for Reference 18

of 'Nonbacterial thrombotic endocarditis'

18
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Libman-Sacks endocarditis and embolic cerebrovascular disease.
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Roldan CA, Sibbitt WL Jr, Qualls CR, Jung RE, Greene ER, Gasparovic CM, Hayek RA, Charlton GA, Crookston K
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JACC Cardiovasc Imaging. 2013 Sep;6(9):973-83.
 
OBJECTIVES: The aim of this study was to determine whether Libman-Sacks endocarditis is a pathogenic factor for cerebrovascular disease (CVD) in systemic lupus erythematosus (SLE).
BACKGROUND: A cardioembolic pathogenesis of SLE CVD manifested as: 1) neuropsychiatric systemic lupus erythematosus (NPSLE), including stroke and transient ischemic attacks (TIA); 2) neurocognitive dysfunction; and 3) magnetic resonance imaging of focal brain lesions has not been established.
METHODS: A 6-year study of 30 patients with acute NPSLE (27 women, 38±12 years of age), 46 age- and sex-matched SLE controls without NPSLE (42 women, 36±12 years of age), and 26 age- and sex-matched healthy controls (22 women, 34±11 years of age) who underwent clinical and laboratory evaluations, transesophageal echocardiography, carotid duplex ultrasound, transcranial Doppler ultrasound, neurocognitive testing, and brain magnetic resonance imaging/magnetic resonance angiography. Patients with NPSLE were re-evaluated after 4.5 months of therapy. All patients were followed clinically for a median of 52 months.
RESULTS: Libman-Sacks vegetations (87%), cerebromicroembolism (27% with 2.5 times more events per hour), neurocognitive dysfunction (60%), and cerebral infarcts (47%) were more common in NPSLE than in SLE (28%, 20%, 33%, and 0%) and healthy controls (8%, 0%, 4%, and 0%, respectively) (all p≤0.009). Patients with vegetations had 3 times more cerebromicroemboli per hour, lower cerebral blood flow, more strokes/TIA and overall NPSLE events, neurocognitive dysfunction, cerebral infarcts, and brain lesion load than those without (all p≤0.01). Libman-Sacks vegetations were independent risk factors of NPSLE (odds ratio [OR]: 13.4; p<0.001), neurocognitive dysfunction (OR: 8.0; p = 0.01), brain lesions (OR: 5.6; p = 0.004), and all 3 outcomes combined (OR: 7.5; p<0.001). Follow-up re-evaluations in 18 of 23 (78%) surviving patients with NPSLE demonstrated improvement of vegetations, microembolism, brain perfusion, neurocognitive dysfunction, and lesion load (all p≤0.04). Finally, patients with vegetations had reduced event-free survival time to stroke/TIA, cognitive disability, or death (p = 0.007).
CONCLUSIONS: The presence of Libman-Sacks endocarditis in patients with SLE was associated with a higher risk for embolic CVD. This suggests that Libman-Sacks endocarditis may be a source of cerebral emboli.
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Division of Cardiology, University of New Mexico School of Medicine and New Mexico VA Health Care Center, Albuquerque, New Mexico. Electronic address: croldan@salud.unm.edu.
PMID