title: Traditional and non-traditional risk factors contribute to the development of accelerated atherosclerosis in patients with systemic lupus erythematosus.
abstract: To determine risk factors of accelerated atherosclerosis in patients with systemic lupus erythematosus (SLE), 72 patients with inactive disease and 36 age- and sex-matched controls were included. The intima-media thickness (IMT) of the common carotid artery was determined by ultrasound. Traditional risk factors and disease-related factors were recorded. Cardiovascular risk was estimated using SCORE (systematic coronary risk evaluation). Markers of inflammation, endothelial activation and vascular remodelling (matrix metalloproteinases (MMP-3, MMP-9) and tissue inhibitor of metalloproteinase- 1 (TIMP- 1)) were determined. IMT was increased in patients (0.67 mm+/-0.13 versus 0.61 mm+/-0.11, P < 0.05). Prevalence of hypertension (33% versus 6%, P < 0.001), SCORE (2.2 (1.7-4.2) versus 1.7 (1.3-2.1), P < 0.001), as well as parameters of inflammation (CRP 1.8 (0.6-5.8) mg/L versus 0.6 (0.2-1.0) mg/L, P < 0.001) and endothelial activation (VCAM-1 505 (389-683) ng/mL versus 374 (322-427) ng/mL, P < 0.001) and von Willebrand factor (138 (59-208)% versus 48 (24-92)%, P < 0.001), were increased in patients. Vascular remodelling was altered: MMP-3 and TIMP-1 were increased (18 (10-29) ng/mL versus 8 (5-11) ng/mL, P < 0.001, and 275 (216-352) ng/mL versus 230 (197-268) ng/mL, P < 0.001, respectively), and MMP-9 was decreased in SLE (266 (147-412) ng/mL versus 348 (226-530) ng/mL, P < 0.05). Univariate analyses revealed that in patients IMT was associated with age, systolic blood pressure, SCORE and disease duration. In multivariate analysis, age and SCORE were independent predictors of IMT. In conclusion, SLE patients have an increased IMT, which is associated with traditional risk factors. Non-traditional risk factors, such as endothelial activation, altered vascular remodelling and disease duration, might play an additional role.
authors.affiliation: Department of Internal Medicine, Division of Clinical Immunology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands. k.de.leeuw@int.umcg.nl
authors.forename: K
authors.initials: K
authors.lastname: de Leeuw
authors.forename: B
authors.initials: B
authors.lastname: Freire
authors.forename: A J
authors.initials: AJ
authors.lastname: Smit
authors.forename: H
authors.initials: H
authors.lastname: Bootsma
authors.forename: C G
authors.initials: CG
authors.lastname: Kallenberg
authors.forename: M
authors.initials: M
authors.lastname: Bijl
mesh_terms: D050197:Atherosclerosis / Q000453:epidemiology* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011859:Radiography; D012307:Risk Factors; D017539:Tunica Intima / Q000000981:diagnostic imaging
chemical_list: D015415:Biomarkers