IntroductionMortality in systemic lupus erythematosus (SLE) patients is influenced by an increased occurrence of severe cardiovascular complications. Statins have been proven to protect a wide spectrum of SLE patients from these complications. This study was conducted to determine the possible efficacy of atorvastatin in SLE patients as assessed by multi-detector computed tomography (MDCT)-based coronary calcium scoring and single photon emission computed tomography (SPECT) of the myocardium.MethodsSixty SLE patients in stable clinical conditions were randomized to receive either atorvastatin (40 mg daily; n = 28) or placebo (n = 32). Clinical and biochemical evaluation together with MDCT-based coronary calcium scoring and SPECT studies (Tc-99 m sestamibi) were performed at the time of randomization and after 1 year of treatment.ResultsAt randomization, SPECT revealed perfusion defects at rest in 22 (36.7%) patients and exercise-induced defects in 8 (13.3%), whereas MDCT revealed coronary calcifications in 15 subjects (25%). Coronary calcium deposits increased after 1 year in the placebo group (plaque volume change from 35.2 ± 44.9 to 62.9 ± 72.4, P < 0.05; calcium score from 32.1 ± 39.1 to 59.5 ± 64.4; P < 0.05), but not in the atorvastatin group (plaque volume 54.5 ± 62.4 vs. 51.0 ± 47.6, P not significant; calcium score 44.8 ± 50.6 vs. 54.9 ± 62.5, P not significant). The atorvastatin group showed a decrease in total serum cholesterol (from 5.1 ± 1.2 to 4.4 ± 0.7 mmol/L, P < 0.05), LDL cholesterol (2.9 ± 1.0 to 2.3 ± 0.6 mmol/L, P < 0.05), triglycerides (1.6 ± 0.6 to 1.2 ± 0.5 mmol/L, P < 0.05), and C-reactive protein (CRP) (4.4 ± 4.1 to 2.7 ± 1.7 mg/L, P < 0.05). There was no change in the mean Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score in patients from both groups. Perfusion defects observed at randomization showed no change after one year treatment with atorvastatin.ConclusionsIn SLE patients 40 mg of atorvastatin daily for 1 year led to a decrease in serum lipids and CRP levels. Additionally the progression of atherosclerosis, as assessed by MDCT-based coronary calcium scoring, is restrained by atorvastatin treatment. The value of statin treatment in patients with SLE free from cardiovascular disease clinical symptoms should be addressed in large, prospective clinical trials.

Conventional risk factors of coronary artery disease fail to explain the increased frequency of cardiovascular morbidity in patients with systemic lupus erythematosus (SLE). The study was conducted to determine possible association between the heart structure and function abnormalities with established prognostic value assessed by non-invasive imaging techniques and markers of autoimmune and inflammatory phenomena typical for SLE. Echocardiography and single photon emission computerized tomography (SPECT; Tc-99m-MIBI) at rest were performed in 60 SLE patients in a stable clinical condition of their disease. Laboratory evaluation included serum levels of C-reactive protein (CRP), complement C3c and C4 components and antiphospholipid antibodies (aPL). The latter included serum anticardiolipin (aCL) and anti-β2-glycoprotein I (antiβ2GPI) antibodies, both of IgG and IgM class, and lupus anticoagulant (LA) in plasma. Echocardiography revealed pathologic thickening of valvular leaflets and/or pericardium in more than 60% of patients. Right ventricular systolic pressure (RVSP) was elevated (>30 mmHg) in 16.7%. Myocardial perfusion defects were present in 36.7% of patients, despite normal ECG recordings and a lack of clinical symptoms of myocardial ischaemia. There was a significant association between thickening of valvular leaflets and/or pericardium and high CRP and low C3c and C4 concentrations. On the other hand, increased RVSP and the presence of myocardial perfusion defects were associated with the presence of anticardiolipin and antiβ2GPI antibodies of the IgG class. Increased anticardiolipin IgG levels predicted perfusion defects in SPECT study with 100% sensitivity and 68% specificity, whereas elevated antiβ2GPI IgG levels predicted RVSP elevation (>30 mmHg) with 100% sensitivity and 78% specificity. In stable SLE patients pericardial and valve abnormalities may be associated with markers of an ongoing inflammation. Also, pulmonary systolic pressure elevation and myocardial perfusion defects are combined with elevated levels of anticardiolipin and antiβ2GPI antibodies of the IgG class. These results indicate that even clinically silent pulmonary hypertension and myocardial perfusion defects in SLE patients could be causally related to the presence of antiphospholipid antibodies.

The aim of this study is to assess the relationship between autoimmunity and endothelial activation/damage (ICAM-1 and vWF serum levels) and the degree of prothrombotic activity (thrombin-antithrombin complexes-TAT serum levels) in SLE. In 60 clinically stable SLE patients, levels of the following parameters were estimated in their serum: lupus anticoagulant (LA), anticardiolipin antibodies in both IgG and IgM classes (aCL-IgG and aCL-IgM, respectively), antiβ2GPI antibodies in both IgG and IgM classes (antiβ2GPI-IgG and antiβ2GPI-IgM, respectively), ICAM, von Willebrand factor (vWF), TAT, CRP, C3c, C4, and IL-6. ICAM-1 values exceeded the upper reference limit in 9 (15%) patients. vWF levels were increased in 21 (35%) patients. In all patients with elevated ICAM-1 values, vWF were also increased. TAT concentrations were elevated in 12 (20%) people. ICAM-1 were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). Similarly, ICAM-1 were significantly higher in patients with elevated antiβ2-GPI-IgM (> 20 SMU vs ≤ 20 SMU; p < 0.05). There was no significant difference in ICAM-1 levels in relation to LA-positivity. vWF were not significantly different in relation to antiphospholipid antibodies nor the inflammation marker levels. TAT were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). In one third of young patients with stable SLE, signs of endothelial activation/damage were found, as shown by elevated plasma ICAM-1 or vWF. Increased prothrombotic tendency manifested by elevated TAT was found in one fifth of the patients. Elevated anticardiolipin (IgM) and anti-β2-glycoprotein I (IgM) antibodies influence endothelial dysfunction and enhance prothrombotic state.

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 one year of follow-up serology tests were performed: anticardiolipin antibodies (aCL), anti-β2 glycoprotein I (aβ2GPI), lupus anticoagulant (LA), C-reactive protein (CRP), soluble form of intracellular adhesion molecule-1 (sICAM-1), vWF:Ag. Results: Coronary artery disease patients in one year follow-up revealed a decrease of aβ2GPI 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 aβ2GPI 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 aβ2GPI IgG level only in CAD patients.

Autoantibodies directed against nuclear protein Ku are infrequently detected. If present, they are found in high titers in patients with connective tissue overlap syndromes. This article describes 5 patients with anti-Ku antibodies in whom systemic lupus erythematosus, Sjögren's syndrome, idiopathic lung fibrosis or scleroderma - polymyositis overlap syndrome were diagnosed. Interestingly, signs and symptoms of transient cranial neuropathy involving trigeminal and facial nerves were reported by 3 patients. Cranial nerve neuropathy has not been described in patients with anti-Ku autoantibodies previously.