title: Relationship of antiphospholipid antibodies to cardiovascular manifestations of systemic lupus erythematosus.
abstract: OBJECTIVE
  Although antiphospholipid antibodies (aPL) are associated with arterial and venous thrombosis in systemic lupus erythematosus (SLE), the extent to which they influence other cardiovascular manifestations is either controversial or uncertain. We undertook this study to examine the relationships of aPL with valvular, myocardial, and arterial disease in SLE.
  
  
  METHODS
  Two hundred patients in an SLE registry, recruited at the time of outpatient visits, underwent comprehensive interviews, physical examinations, laboratory assessments, echocardiography to assess left ventricular (LV) and valvular status, carotid ultrasonography to detect atherosclerosis (discrete plaque), and radial applanation tonometry to measure arterial stiffness.
  
  
  RESULTS
  Antiphospholipid antibodies were present(defined as IgG or IgM anticardiolipin > or =40 IU/ml or the presence of lupus anticoagulant) in 42 patients (21%). Mitral valve nodules and moderate-to-severe mitral regurgitation were more common in aPL-positive patients (both 14.3% versus 4.4%; P = 0.02). Thirty-one percent of patients with high titers of IgG aPL (>80 IU/ml) had mitral valve nodules, compared with 20% of patients with mildly to moderately elevated levels of IgG aPL (16-80 IU/ml) and 4% of patients without IgG aPL (overall P < 0.001). Levels of soluble tumor necrosis factor receptors were higher in the presence of both aPL and mitral valve nodules. LV dimensions, systolic function, and carotid artery stiffness as well as prevalences of Raynaud's phenomenon, pulmonary hypertension, and atherosclerosis were similar in aPL-positive and aPL-negative patients.
  
  
  CONCLUSIONS
  Antiphospholipid antibodies in SLE are associated with mitral valve nodules and significant mitral regurgitation, possibly due to valvular endothelial cell activation. However, in this population, they are not associated with evidence of myocardial hypertrophy, systolic dysfunction, coronary or carotid atherosclerosis, or other vascular abnormalities.
authors.affiliation: Hospital for Special Surgery, Weill Medical College of Cornell University, New York, New York 10021, USA.
authors.forename: Afshin
authors.initials: A
authors.lastname: Farzaneh-Far
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Roman
authors.forename: Michael D
authors.initials: MD
authors.lastname: Lockshin
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Paget
authors.forename: Mary K
authors.initials: MK
authors.lastname: Crow
authors.forename: Adrienne
authors.initials: A
authors.lastname: Davis
authors.forename: Lisa
authors.initials: L
authors.lastname: Sammaritano
authors.forename: Daniel M
authors.initials: DM
authors.lastname: Levine
authors.forename: Jane E
authors.initials: JE
authors.lastname: Salmon
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D002318:Cardiovascular Diseases / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D004452:Echocardiography; D005260:Female; D006304:Health Status; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008943:Mitral Valve / Q000473:pathology / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000150:complications / Q000276:immunology / Q000503:physiopathology; D012720:Severity of Illness Index
chemical_list: D017153:Antibodies, Anticardiolipin; D007074:Immunoglobulin G; D007075:Immunoglobulin M