Influence of statin therapy on antiphospholipid antibodies and endothelial dysfunction in young patients with coronary artery disease and systemic lupus erythematosus

Introduction: Antiphospholipid antibodies (aPL) affect atherogenesis and may cause thromboembolism in systemic lupus erythematosus (SLE) and coronary artery disease (CAD). Intensive treatment with statins may reduce inflammation and decrease the number of thrombotic events. That may explain the beneficial effect of statin therapy in SLE and CAD. This study was established to investigate the influence of statin treatment on aPL antibody levels and selected endothelial dysfunction markers in CAD and SLE patients. Material and methods: Fifty-eight patients - 40 after coronary revascularization (age 38.9 (27-46), 35 males) and 18 with clinically stable SLE (age 38.8 (18-62), 1 male) - were enrolled in the study. In both groups intensive atorvastatin treatment was administered. At baseline and after 1 year of follow-up serology tests were performed: anticardiolipin antibodies (aCL), anti-beta 2 glycoprotein I (a beta 2GPI), lupus anticoagulant (LA), C-reactive protein (CRP), soluble form of intracellular adhesion molecule-1 (sICAM-1), vWF:Ag. Results: Coronary artery disease patients in 1 year follow-up revealed a decrease of a beta 2GPI IgG and CRP. There was a significant increase in aCL IgG, sICAM-1 and vWF:Ag. In SLE patients aPL levels showed no significant reduction after treatment. Conclusions: In clinically stable patients IgM and IgG class a beta 2GPI levels are higher in CAD than in SLE, whereas IgG class aCL levels are lower. Statin treatment decreases the CRP level in both SLE and CAD patients, while decreasing the a beta 2GPI IgG level only in CAD patients.