FRI0277 Arterial stiffness in systemic lupus erythematosus (SLE) patients: a controlled study

Background Arterial stiffness reflects changes in mechanical properties of vascular wall that occurs early with onset of vascular disease and may be a reliable surrogate marker for cardiovascular disease (CVD) in SLE (1,2). Objectives To characterize the role for traditional and non-traditional CVD...

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Published inAnnals of the rheumatic diseases Vol. 72; no. Suppl 3; p. A468
Main Authors Sacre, K., Escoubet, B., Chauchard, M., Chauveheid, M.-P., Zennaro, M.-C., Papo, T.
Format Journal Article
LanguageEnglish
Published London BMJ Publishing Group Ltd and European League Against Rheumatism 01.06.2013
BMJ Publishing Group LTD
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Summary:Background Arterial stiffness reflects changes in mechanical properties of vascular wall that occurs early with onset of vascular disease and may be a reliable surrogate marker for cardiovascular disease (CVD) in SLE (1,2). Objectives To characterize the role for traditional and non-traditional CVD risk factors on arterial stiffness in SLE patients and if and how arterial stiffness impacts on SLE-associated feature such as renal function. Methods Carotid-femoral pulse wave velocity (PWV) was prospectively assessed as a measure for arterial stiffness in 42 SLE patients asymptomatic for CVD and 36 age- and sex-matched controls. Vascular disease evaluation included measurements of brachial pulse pressure (PP), common carotid artery intima-media thickness (IMT), and internal carotid artery wall thickness (ICWT). Risk factors for CVD and SLE disease history were analyzed. Results Forty-two SLE patients and 36 controls were studied. All SLE patients were receiving hydroxychloroquine. All received long-term glucocorticoids and 28 (66.7%) were still under prednisone at a mean daily dose of 9 mg (range: 5-17) at study time. Twenty-eight received immunosuppressive or immunomodulatory drugs at some points during follow-up. Five patients had antiphospholipid syndrome. Classical cardiovascular risks distribution did not differ between controls and SLE patients (Table 1) PWV was higher in SLE patients than controls (7.1 ±1.6 m/s vs 6.4 + 1 m/s; p=0.03) and correlated with PP (r2=0.21, p=0.002), IMT (r2=0.11, p=0.03) and ICWT (r2=0.39, p<0.0001). PWV was associated with older age (r2=0.21, p=0.002), higher systolic blood pressure (SBP) (r2=0.44, p<0.0001) and higher cumulative glucocorticoid therapy (r2=0.14, p=0.01). The impact of SBP on PWV was higher in SLE patients than controls (p=0.0004). Eventually, impaired renal function assessed by the reduction of glomerular rate filtration correlated with PWV in SLE (r=-0.52, p=0.0004). No statistical relationship was found between PWV and Framingham score, body mass index, SELENA SLEDAI score, duration of SLE disease, cholesterol, HbA1c, homocystein and, 25(OH)-D3 vitamin. Conclusions Despite a low risk for CVD according to traditional factors, PWV was higher in SLE patients as compared to controls. Age, SBP and glucocorticoid therapy are associated with increased arterial stiffness. Conversely, arterial stiffness contributes to alter renal function in SLE patients. References Cacciapaglia F, et al. Lupus 2009;18:249-256 Chin CW, et al. Clin Exp Rheumatol 2012 [Epub ahead of print] Disclosure of Interest: None Declared
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ISSN:0003-4967
1468-2060
DOI:10.1136/annrheumdis-2013-eular.1404