Endothelial Dysfunction,clinical corelation and atorvastatin therapy in patients with systemic lupus erythematosus |
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| Affiliation: | 1. Department of Rheumatology and Internal Medicine Medical Clinic II;2. Department of Internal Medicine Medical Clinic IV;3. Department of Radiology, Department of Computer Science and Statistics, University of Medicine Cluj, Romania;1. Department of Medicine, Karolinska Institutet and Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden;2. NARILIS, URBC, University of Namur, Namur, Belgium;3. Department of Pharmacy, Namur Thrombosis and Hemostasis Center, University of Namur, Namur, Belgium;1. Department of Clinical and Molecular Biomedicine, Catania University, Catania, Italy;2. Université Paris-Est, UMR_S955, UPEC, F-94000 Créteil, France;3. Inserm U955, Equipe 3, F-94000 Créteil, France;1. Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, Texas Southern University, Houston, TX 77004, USA;2. Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University, Omaha, NE 68178, USA;3. University of Exeter Medical School, St. Luke''s Campus, Magdalen Road, Exeter EX1 2LU, UK;4. Department of Biosciences, College of Life and Environmental Sciences, University of Exeter, UK;1. Ludwig Boltzmann Institute for Rheumatology and Balneology, Cluster Rheumatology, Balneology and Rehabilitation, Vienna, Austria;2. Department of Pharmacology and Toxicology, Karl-Franzens-University Graz, Graz, Austria;3. Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria;1. Department of Allergy and Immunology, The Children''s Hospital at Westmead, Sydney;2. Discipline of Paediatrics and Child Health, Sydney Medical School, University of Sydney;1. Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA;2. Cardiovascular and Metabolic Research Unit, Lakehead University, Thunder Bay, ON, Canada;3. Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, MD, USA;4. Division of Pulmonary, Allergy and Critical Care, Airways Biology Initiative, University of Pennsylvania Medical Center, Philadelphia, PA, USA;5. Department of Biology, Lakehead University, Thunder Bay, ON, Canada |
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| Abstract: | BackgroundSystemic lupus erythematosus (SLE) patients have a significantly increased risk cardiovascular morbidity and mortality that are not fully explained by classic risk factors. Endothelial dysfunction is an early stage in the process of atherogenesis and the first step is decrease of endothelium dependent vasodilatation.ObjectivesThe aim of the present study was to determine endothelial dysfunction in lupus patients, to compare to healthy volunteers and to correlate the results with the disease activity and laboratory markers and to evaluate atorvastatin efficacy in improving vasodilatation in SLE patients.Methods20 SLE women and 20 healthy female subjects were assessed by non-invasive ultrasound on the brachial artery. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation (FMD) in response to reactive hyperemia (induced by 5 minutes compression) and nitroglycerin dilatation, respectively. A complete history, physical examination were performed and disease activity were assessed by the SLE Disease Activity Index (SLEDAI).Conventional risk factors for coronary heart disease, Raynaud's phenomenon, previous thrombosis, cardiovascular event, lipid profile, complement levels, antibodies to ds-DNA, anti-phospholipid antibodies were recorded.LES patients received atorvastain 80 mg/day during eight weeks and endothelium-dependent and independent function were evaluated at baseline and at the end of the study.ResultsMedian age was 38 years; disease duration of SLE patients was 8 years (range 1 to 20 years). The patients show lupus activity ranging from 2 – 44 points in SLEDAI scale. The SLE patients had impaired flow-mediated dilation of the brachial artery compared with control subjects (9.6%; range 5.8% to 15.9% versus 26.5%; range 23.1% to 30.3% P<0.01) but preserved nitroglycerin dilation. Traditional cardiovascular risk factors were similar in both groups. The FMD correlated positively with SLEDAI, lupus anticoagulant and Raynauds phenomenon, but there were no correlation between FMD and anticardiolipin antibodies or low complement.Atorvastatin was associated with semnificativ increase in flow mediated dilatation in LES patient (4%, range 2,9-8,2 versus 7,3, range 4,3-10,2), p<0.001.ConclusionImpaired endothelial function in SLE seems to be correlate with disease activity. Improving endothelial function may therefore have an impact on the risk of future cardiovascular disease and statins could be a good therapy. |
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