Libman-Sacks endocarditis and embolic cerebrovascular disease
| Autor: | Carlos A. Roldan, Charles Gasparovic, Wilmer L. Sibbitt, Gerald A. Charlton, Kendall P. Crookston, Ernest R. Greene, Clifford Qualls, Reyaad A. Hayek, Rex E. Jung |
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| Rok vydání: | 2013 |
| Předmět: |
Adult
Male medicine.medical_specialty Ultrasonography Doppler Transcranial 030204 cardiovascular system & hematology Libman–Sacks endocarditis Magnetic resonance angiography 03 medical and health sciences 0302 clinical medicine Risk Factors Internal medicine medicine Endocarditis Humans Lupus Erythematosus Systemic Radiology Nuclear Medicine and imaging Stroke Retrospective Studies 030203 arthritis & rheumatology Libman-Sacks endocarditis medicine.diagnostic_test transesophageal echocardiography business.industry Magnetic resonance imaging Odds ratio Middle Aged medicine.disease Prognosis stroke Magnetic Resonance Imaging cerebrovascular disease 3. Good health Transcranial Doppler Cerebral blood flow Intracranial Embolism Radiology Nuclear Medicine and imaging Cardiology microembolism Female business Cardiology and Cardiovascular Medicine Echocardiography Transesophageal Follow-Up Studies |
| Zdroj: | JACC. Cardiovascular imaging. 6(9) |
| ISSN: | 1876-7591 |
| Popis: | ObjectivesThe aim of this study was to determine whether Libman-Sacks endocarditis is a pathogenic factor for cerebrovascular disease (CVD) in systemic lupus erythematosus (SLE).BackgroundA 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.MethodsA 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.ResultsLibman-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).ConclusionsThe 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. |
| Databáze: | OpenAIRE |
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