scholarly journals Semiquantified Noncalcified Coronary Plaque in Systemic Lupus Erythematosus

2012 ◽  
Vol 39 (12) ◽  
pp. 2286-2293 ◽  
Author(s):  
ADNAN N. KIANI ◽  
JENS VOGEL-CLAUSSEN ◽  
ARMIN ARBAB-ZADEH ◽  
LAURENCE S. MAGDER ◽  
JOAO LIMA ◽  
...  

Objective.A major cause of morbidity and mortality in systemic lupus erythematosus (SLE) is accelerated coronary atherosclerosis. New technology (computed tomographic angiography) can measure noncalcified coronary plaque (NCP), which is more prone to rupture. We report on a study of semiquantified NCP in SLE.Methods.Patients with SLE (n = 147) with no history of cardiovascular disease underwent 64-slice coronary multidetector computed tomography (MDCT). The MDCT scans were evaluated quantitatively by a radiologist, using dedicated software.Results.The group of 147 patients with SLE was 86% female, 70% white, 29% African American, and 3% other ethnicity. The mean age was 51 years. In our univariate analysis, the major traditional cardiovascular risk factors associated with noncalcified plaque were age (p = 0.007), obesity (p = 0.03; measured as body mass index), homocysteine (p = 0.05), and hypertension (p = 0.04). Anticardiolipin (p = 0.026; but not lupus anticoagulant) and anti-dsDNA (p = 0.03) were associated with higher noncalcified plaque. Prednisone and hydroxychloroquine therapy had no effect, but methotrexate (MTX) use was associated with higher noncalcified plaque (p = 0.0001). In the best multivariate model, age, current MTX use, and history of anti-dsDNA remained significant.Conclusion.Our results suggest that serologic SLE (anti-dsDNA) and traditional cardiovascular risk factors contribute to semiquantified noncalcified plaque in SLE. The association with MTX is not understood, but should be replicated in larger studies and in multiple centers.

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Brygida Przywara-Chowaniec ◽  
Dominika Blachut ◽  
Jan Harpula ◽  
Marcin Bereś ◽  
Agnieszka Nowak ◽  
...  

Systemic lupus erythematosus is a rare autoimmune disease. It leads to an increased production of proinflammatory molecules that accelerates atherogenesis and could cause an endothelium dysfunction. The aim of the study was to assess cardiovascular risk factors such as BMI and lipid profile as well as left ventricular ejection fraction among patients with SLE, and a correlation of these factors with duration of the disease. Materials and Methods. The researched group consisted of patients with SLE, being under control of the outpatient clinic of cardiology. This group included 38 patients among whom 34 were women (56.17 ± 11.05 years) and 4 were men (65.50 ± 9.22 years). The control group consisted of 19 healthy women (53.31 ± 11.94 years) and 2 healthy men (38.51 ± 7.53 years). Measurements were taken in the same conditions by trained medical staff. Results. Excessive body weight (BMI >25 kg/m2) was more frequent in the SLE group, but it was not statistically significant (55.26% vs. 52.38%, p = 0.6159 ). LVEF values were lower in their searched group, and this factor showed statistical significance (53.92% ± 6.46 vs. 58.67% ± 4.69, p = 0.0044 ). Thickness of the IMT was higher and statistically important among patients with SLE, both in left (1.22 ± 0.27 mm vs. 0.7 ± 0.21 mm, p = 0.0001 ) and right common carotid artery (1.16 ± 0.26 mm vs. 0.59 ± 0.15 mm, p = 0.0001 ), compared to the controls. Conclusions. Patients with SLE are at greater risk of developing cardiovascular diseases as the illness progresses. The activity of the disease according to the SLEDAI-2K scale may have an impact on the LVEF values which was significantly decreased in the group with active disease, but further thorough investigation is required to fully evaluate the impact of individual components of the disease and its treatment on the CVD development and mortality.


2019 ◽  
Vol 15 (3) ◽  
pp. 177-188 ◽  
Author(s):  
Edoardo Sciatti ◽  
Ilaria Cavazzana ◽  
Enrico Vizzardi ◽  
Ivano Bonadei ◽  
Micaela Fredi ◽  
...  

Background: Accelerated atherosclerosis, responsible for premature cardiovascular disease, has been estimated to develop or progress in 10% of systemic lupus erythematosus (SLE) patients each year and to be 6-fold more frequent in SLE compared with the general population. The mechanisms underlying accelerated atherosclerosis in SLE are complex and involve classical and “non-classical” cardiovascular risk factors. Subclinical and disseminated atherosclerosis is associated with endothelial dysfunction and arterial stiffness. Objective: The aim of this review is to analyze the association between SLE and endothelial dysfunction. Results and Conclusion: Different mechanisms have been proposed to explain the prevalence of endothelial dysfunction in SLE, which are briefly reported in this review: impaired clearance of apoptotic cells, oxidative stress markers, B cell activation with different circulating autoantibodies, different subtypes of T lymphocytes, cytokine cascade. Several studies and meta-analyses show a significant trend towards a prevalence of subclinical accelerated atherosclerosis in patients with SLE compared with healthy controls, since childhood. Based on general considerations, we suggest a multidisciplinary management to assess endothelial dysfunction at the diagnosis of the disease and to periodically search for and treat the traditional cardiovascular risk factors. Prospective studies are needed to confirm the benefits of this management.


Lupus ◽  
2020 ◽  
Vol 29 (14) ◽  
pp. 1866-1872
Author(s):  
Lucila Garcia ◽  
Maria S Velloso ◽  
Maria V Martire ◽  
Florencia Savy ◽  
Fernando Arizpe ◽  
...  

Introduction Assessment of risk both for pregnancy morbidity and thrombosis in the presence of anti-phospholipid antibodies (aPL) is still a challenge in Systemic Lupus Erythematosus (SLE) patients. The Global Antiphospholipid Syndrome Score (GAPSS) takes into account the aPL profile (criteria and non-criteria aPL), the conventional cardiovascular risk factors and the autoimmune antibody profile. An adjusted model of the score (aGAPSS) excluding anti-phosphatidylserine/Prothrombin (aPS/PT), suggests that the score is able to stratify patients for their rate of events making it widely applicable in daily clinical practice. Objective To validate the aGAPSS in a multicentric cohort of SLE patients in Argentina. Patients and methods consecutive SLE patients with and with andwithout thrombotic events from seven Rheumatologist centers were included. Traditional cardiovascular risk factors, aPL antibodies and medications received (aspirin, hydroxychloroquine and anticoagulation) were collected. The score aGAPSS was calculated for each patient at the last visit by adding together the points corresponding to the risk factors: 1 for hypertension, 3 for dyslipidemia, 4 for LA and B2GPI (IgM or IgG) antibodies and 5 for aCL (IgM or IgG) antibodies. The discriminative ability of the aGAPSS was calculated by measuring the area under the receiver operating characteristic curve (AUC). Multivariate logistic regression analysis was performed to examine the impact of multiple cardiovascular risk factors and laboratory parameters on the occurrence of thrombosis. Results Two hundred and ninety-six SLE patients were included. One-hundred and twenty-one patients (40.9%) presented thrombotic and/or pregnancy complications. Median aGAPSS was significantly higher in patients who experienced an event (thrombosis and/or pregnancy morbidity) compared with those without [4 (IQR 1–9) versus 1 (IQR 0–5); p < 0.001]. The best cut off point for the diagnosis of thrombosis and/or pregnancy complications was aGAPSS ≥4. Multivariate logistic regression analysis showed that aCL antibodies [OR 2.1 (95% CI 1.16–3.90); p = 0.015] were an independent risk factors for thrombotic events. Conclusions This score is a simple tool, easy to apply to SLE patients in daily practice. The use of the aGAPSS could change the non-pharmacologic and pharmacologic treatment in higher risk patients to improve their survival.


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