scholarly journals Low Socioeconomic Status Is Associated with Cardiovascular Risk Factors and Outcomes in Systemic Lupus Erythematosus

2012 ◽  
Vol 39 (4) ◽  
pp. 777-783 ◽  
Author(s):  
JANET W. MAYNARD ◽  
HONG FANG ◽  
MICHELLE PETRI
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Socioeconomic Status ◽  
Cardiovascular Risk ◽  
African Americans ◽  
Cardiovascular Risk Factors ◽  
Low Income ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Low Education

Objective.Accelerated atherosclerosis is a major cause of death in systemic lupus erythematosus (SLE), yet little is known about the effect of socioeconomic status. We investigated whether education or income levels are associated with cardiovascular risk factors and outcomes in SLE.Methods.Our study involved a longitudinal cohort of all patients with SLE enrolled in the Hopkins Lupus Cohort from 1987 through September 2011. Socioeconomic status was measured by education level (≥ 12 years or < 12) and income tertiles (> $60,000, $25,000–$60,000, or < $25,000).Results.A total of 1752 patients with SLE were followed prospectively every 3 months. There were 1052 whites and 700 African Americans. Current smoking, obesity, hypertension, and diabetes mellitus were more common in African Americans (p < 0.01 for all), but there was no statistical difference in the frequency of myocardial infarction or stroke. In multivariate analyses stratified by ethnicity, low income was strongly associated with most traditional cardiovascular risk factors in whites, but only with smoking and diabetes in African Americans. In whites, low income increased the risk of both myocardial infarction (OR 3.24, 95% CI 1.41–7.45, p = 0.006) and stroke (OR 2.85, 95% CI 1.56–5.21, p = 0.001); in African Americans, these relationships were not seen. Low education, in contrast, was associated with smoking in both ethnic groups.Conclusion.Low income, not low education, is the socioeconomic status variable associated with cardiovascular risk factors and events. This association is most clearly demonstrable in whites.

Abstract MP47: The Association of Socioeconomic Status with Subclinical Myocardial Damage

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Anna E Fretz ◽  
Andrea L Schneider ◽  
John McEvoy ◽  
Ron Hoogeveen ◽  
Christie M Ballantyne ◽  
...  
Keyword(s):  
Risk Factors ◽  
Socioeconomic Status ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Low Income ◽  
Myocardial Damage ◽  
Low Ses ◽  
12Th Grade ◽  
Low Education ◽  
Prevalence Ratios

Background: The association between socioeconomic status (SES) and clinical cardiovascular events is well established. However, little is known about the relationship between SES and subclinical myocardial damage, as assessed by a novel highly sensitive assay for cardiac troponin T (hs-cTnT). Methods: We conducted a cross-sectional analysis of 11,411 participants from the ARIC Study with no history of cardiovascular disease who had hs-cTnT measured at visit 2 (1990-1992). SES was defined using either annual household income, categorized as: low (<$16,000), mid-level ($16,000 - $34,999), high (≥ $35,000), or lifetime educational attainment, categorized as: low (<12th grade), mid-level (12th grade/some college) and high (college degree or higher). hs-cTnT was categorized as non-elevated (<14 ng/L) and elevated (≥ 14ng/L). Poisson regression was used to generate prevalence ratios for elevated hs-cTnT, separately by level of income and education after adjusting for demographic, clinical, and behavioral factors. Results: Persons with low income or low education were more likely to have subclinical myocardial damage as assessed by elevated hs-cTnT (≥14ng/L). Adjusted prevalence ratios for elevated troponin comparing low to high levels of income and education were 1.74 (95% CI: 1.32, 2.29) and 1.54 (95% CI: 1.21, 1.97), respectively (Table, Model 1). These results were slightly attenuated, but remained statistically significant after adjusting for cardiovascular risk factors and health behaviors (Models 2 and 3). Race-stratified results demonstrate a somewhat stronger and only significant association of low education with subclinical myocardial damage in blacks compared to whites (PR 1.83 vs 1.05, p-interaction =0.08). There was no race interaction with income (p-interaction =0.33). Conclusions: Low SES was associated with elevated hs-cTnT, independent of cardiovascular risk factors, especially in blacks. Further research is needed to explore how low SES contributes to subclinical myocardial damage.

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 ◽  
...  
Keyword(s):  
Risk Factors ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Lupus Erythematosus ◽  
Univariate Analysis ◽  
Coronary Plaque ◽  
Systemic Lupus ◽  
History Of ◽  
Noncalcified Plaque

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.

scholarly journals Systemic Lupus Erythematosus, Its Impact on Selected Cardiovascular Risk Factors, and Correlation with Duration of Illness: A Pilot Study

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Brygida Przywara-Chowaniec ◽  
Dominika Blachut ◽  
Jan Harpula ◽  
Marcin Bereś ◽  
Agnieszka Nowak ◽  
...  
Keyword(s):  
Risk Factors ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Lupus Erythematosus ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Systemic Lupus ◽  
Ventricular Ejection Fraction ◽  
The Impact

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.

Systemic Lupus Erythematosus and Endothelial Dysfunction: A Close Relationship

2019 ◽  
Vol 15 (3) ◽  
pp. 177-188 ◽  
Author(s):  
Edoardo Sciatti ◽  
Ilaria Cavazzana ◽  
Enrico Vizzardi ◽  
Ivano Bonadei ◽  
Micaela Fredi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Risk ◽  
Endothelial Dysfunction ◽  
Cardiovascular Risk Factors ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
Systemic Lupus ◽  
Accelerated Atherosclerosis ◽  
Premature Cardiovascular Disease

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.

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