title: Libman-Sacks endocarditis and embolic cerebrovascular disease.
abstract: OBJECTIVE
  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.
authors.affiliation: 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.
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Roldan
authors.forename: Wilmer L
authors.initials: WL
authors.lastname: Sibbitt
authors.forename: Clifford R
authors.initials: CR
authors.lastname: Qualls
authors.forename: Rex E
authors.initials: RE
authors.lastname: Jung
authors.forename: Ernest R
authors.initials: ER
authors.lastname: Greene
authors.forename: Charles M
authors.initials: CM
authors.lastname: Gasparovic
authors.forename: Reyaad A
authors.initials: RA
authors.lastname: Hayek
authors.forename: Gerald A
authors.initials: GA
authors.lastname: Charlton
authors.forename: Kendall
authors.initials: K
authors.lastname: Crookston
mesh_terms: D000328:Adult; D017548:Echocardiography, Transesophageal; D004696:Endocarditis / Q000150:complications* / Q000175:diagnosis; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D020766:Intracranial Embolism / Q000175:diagnosis / Q000209:etiology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000175:diagnosis; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D017585:Ultrasonography, Doppler, Transcranial
keywords: CVD; Libman-Sacks endocarditis; MRA; NPSLE; SLE; TEE; TIA; TTE; cerebrovascular disease; magnetic resonance angiography; microembolism; neuropsychiatric systemic lupus erythematosus; stroke; systemic lupus erythematosus; transesophageal echocardiography; transient ischemic attack; transthoracic echocardiography
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