Vascular Disease in Systemic Lupus Erythematosus (original) (raw)
Cardiovascular Events in Systemic Lupus Erythematosus
Medicine, 2015
This article estimates the frequency of cardiovascular (CV) events that occurred after diagnosis in a large Spanish cohort of patients with systemic lupus erythematosus (SLE) and investigates the main risk factors for atherosclerosis. RELESSER is a nationwide multicenter, hospital-based registry of SLE patients. This is a cross-sectional study. Demographic and clinical variables, the presence of traditional risk factors, and CV events were collected. A CV event was defined as a myocardial infarction, angina, stroke, and/or peripheral artery disease. Multiple logistic regression analysis was performed to investigate the possible risk factors for atherosclerosis. From 2011 to 2012, 3658 SLE patients were enrolled. Of these, 374 (10.9%) patients suffered at least a CV event. In 269 (7.4%) patients, the CV events occurred after SLE diagnosis (86.2% women, median [interquartile range] age 54.9 years [43.2-66.1], and SLE duration of 212.0 months [120.8-289.0]). Strokes (5.7%) were the most frequent CV event, followed by ischemic heart disease (3.8%) and peripheral artery disease (2.2%). Multivariate analysis identified age (odds ratio [95% confidence interval], 1.03 [1.02-1.04]), hypertension (1.71 [1.20-2.44]), smoking (1.48 [1.06-2.07]), diabetes (2.2 [1.32-3.74]), dyslipidemia (2.18 [1.54-3.09]), neurolupus (2.42 [1.56-3.75]), valvulopathy (2.44 [1.34-4.26]), serositis (1.54 [1.09-2.18]), antiphospholipid antibodies (1.57 [1.13-2.17]), low complement (1.81 [1.12-2.93]), and azathioprine (1.47 [1.04-2.07]) as risk factors for CV events. We have confirmed that SLE patients suffer a high prevalence of premature CV disease. Both traditional and nontraditional risk factors contribute to this higher prevalence. Although it needs to be verified with future studies, our study also shows-for the first time-an association between diabetes and CV events in SLE patients.
Atherosclerotic vascular events in a multinational inception cohort of systemic lupus erythematosus
Arthritis Care & Research, 2010
ObjectiveTo describe vascular events during an 8-year followup in a multicenter systemic lupus erythematosus (SLE) inception cohort and their attribution to atherosclerosis.To describe vascular events during an 8-year followup in a multicenter systemic lupus erythematosus (SLE) inception cohort and their attribution to atherosclerosis.MethodsClinical data, including comorbidities, were recorded yearly. Vascular events were recorded and attributed to atherosclerosis or not. All of the events met standard clinical criteria. Factors associated with atherosclerotic vascular events were analyzed using descriptive statistics, t-tests, and chi-square tests. Stepwise multivariate logistic regression was used to assess the association of factors with vascular events attributed to atherosclerosis.Clinical data, including comorbidities, were recorded yearly. Vascular events were recorded and attributed to atherosclerosis or not. All of the events met standard clinical criteria. Factors associated with atherosclerotic vascular events were analyzed using descriptive statistics, t-tests, and chi-square tests. Stepwise multivariate logistic regression was used to assess the association of factors with vascular events attributed to atherosclerosis.ResultsSince 2000, 1,249 patients have been entered into the cohort. There have been 97 vascular events in 72 patients, including: myocardial infarction (n = 13), angina (n = 15), congestive heart failure (n = 24), peripheral vascular disease (n = 8), transient ischemic attack (n = 13), stroke (n = 23), and pacemaker insertion (n = 1). Fifty of the events were attributed to active lupus, 31 events in 22 patients were attributed to atherosclerosis, and 16 events were attributed to other causes. The mean ± SD time from diagnosis to the first atherosclerotic event was 2.0 ± 1.5 years. Compared with patients followed for 2 years without atherosclerotic events (n = 615), at enrollment, patients with atherosclerotic vascular events were more frequently white, men, older at diagnosis of SLE, obese, smokers, hypertensive, and had a family history of coronary artery disease. On multivariate analysis, only male sex and older age at diagnosis were associated factors.Since 2000, 1,249 patients have been entered into the cohort. There have been 97 vascular events in 72 patients, including: myocardial infarction (n = 13), angina (n = 15), congestive heart failure (n = 24), peripheral vascular disease (n = 8), transient ischemic attack (n = 13), stroke (n = 23), and pacemaker insertion (n = 1). Fifty of the events were attributed to active lupus, 31 events in 22 patients were attributed to atherosclerosis, and 16 events were attributed to other causes. The mean ± SD time from diagnosis to the first atherosclerotic event was 2.0 ± 1.5 years. Compared with patients followed for 2 years without atherosclerotic events (n = 615), at enrollment, patients with atherosclerotic vascular events were more frequently white, men, older at diagnosis of SLE, obese, smokers, hypertensive, and had a family history of coronary artery disease. On multivariate analysis, only male sex and older age at diagnosis were associated factors.ConclusionIn an inception cohort with SLE followed for up to 8 years, there were 97 vascular events, but only 31 were attributable to atherosclerosis. Patients with atherosclerotic events were more likely to be men and to be older at diagnosis of SLE.In an inception cohort with SLE followed for up to 8 years, there were 97 vascular events, but only 31 were attributable to atherosclerosis. Patients with atherosclerotic events were more likely to be men and to be older at diagnosis of SLE.
Update on vascular disease in systemic lupus erythematosus
Current Opinion in Rheumatology, 2003
Purpose of review Young women with systemic lupus erythematosus have strikingly high rates of coronary heart disease. Current knowledge indicates that atherosclerosis is an active inflammatory and immune-mediated process. Therefore, the chronic inflammation and immune dysregulation characteristic of systemic lupus erythematosus undoubtedly contribute to the accelerated vascular disease seen in these patients. Carefully considering what is known about atherogenesis in the general population will provide clues to unraveling the complexity of why systemic lupus erythematosus and atherosclerosis are linked so frequently. Recent findings Inflammation is involved in all aspects of atherogenesis from the initial endothelial "response to injury," to foam cell formation leading to the atherosclerotic lesion, to the rupture of the "vulnerable" fibrous cap, resulting in the acute coronary syndrome and potentially in death. The authors review how factors commonly seen in systemic lupus erythematosus or inherent to the underlying disease mechanism may contribute to each of the stages of atherogenesis. Summary Our focus on the causes of vascular disease in systemic lupus erythematosus must now include nontraditional risk factors such as immune and inflammatory mediators. With the advent of noninvasive screening tools for atherosclerosis, we are better equipped to measure subclinical vascular disease and associated risk factors, including immune and inflammatory mediators. When considering strategies for preventing premature cardiovascular disease in systemic lupus erythematosus, modifying immune and inflammatory risk factors will likely become a major component of the program in addition to modifying the current traditional risk factors.
Arthritis Research & Therapy, 2009
Introduction Cardiovascular disease (CVD) is a major cause of premature mortality among Systemic lupus erythematosus (SLE) patients. Many studies have measured and evaluated risk factors for premature subclinical atherosclerosis, but few studies are prospective and few have evaluated risk factors for hard endpoints, i.e. clinically important cardiovascular events (CVE). We investigated the impact of traditional and lupus associated risk factors for the first ever CVE in a longitudinal cohort of SLE patients.
Systemic lupus erythematosus and thrombosis
Thrombosis Journal, 2015
Systemic Lupus Erythematosus (SLE) is an acquired, multiorgan, autoimmune disease. Clinical presentation is extremely variable and heterogeneous. It has been shown that SLE itself is an independent risk factor for developing both arterial and venous thrombotic events since SLE patients have an Odds Ratio (OR) for thrombosis that varies depending on the clinical and laboratory characteristics of each study cohort. The risk of developing a thrombotic event is higher in this setting than in the general population and may further increase when associated with other risk factors, or in the presence of inherited or acquired pro-thrombotic abnormalities, or trigger events. In particular, a striking increase in the number of thrombotic events was observed when SLE was associated with antiphospholipid antibodies (aPL). The presence of aPLs has been described in about 50% of SLE patients, while about 20% of antiphospholipid syndrome (APS) patients have SLE. While APS patients (with or without an autoimmune disease) have been widely studied in the last years, fewer studies are available for SLE patients and thrombosis in the absence of APS. Although the available literature undoubtedly shows that SLE patients have a greater prevalence of thrombotic events as compared to healthy subjects, it is difficult to obtain a definite result from these studies because in some cases the study cohort was too small, in others it is due to the varied characteristics of the study population, or because of the different (and very copious) laboratory assays and methods that were used. When an SLE patient develops a thrombotic event, it is of great clinical relevance since it is potentially life-threatening. Moreover, it worsens the quality of life and is a clinical challenge for the clinician.
Under crossfire: thromboembolic risk in systemic lupus erythematosus
Rheumatology
Cerebral and cardiovascular ischaemic events are frequent complications of systemic lupus erythematosus (SLE) and constitute primary causes of permanent damage. However, the pathogenic determinants of an increased thromboembolic risk in patients with SLE are only partially understood. Atherosclerosis constitutes a fertile soil for the development of thrombosis and shows disproportionately high prevalence and progression rates in patients with SLE. Antiphospholipid antibodies are independent risk factors for acute thrombosis, but can also prompt long-term vascular inflammation. Aberrant interactions among immune cells and dysfunctions in the deployment of the coagulation cascade have historically less been explored in SLE, but recent evidence suggests they can also play a critical role at the crossroads between inflammation and haemostasis. In this review, we discuss how different pro-thrombotic mechanisms can be prompted by and synergise with SLEspecific pathogenic events and speculate about novel potential directions for research and drug development.
Atherosclerotic vascular disease in systemic lupus erythematosus
Journal of the National Medical Association, 2002
In the United States, systemic lupus erythematosus (SLE) disproportionately affects African Americans. It has become a chronic disease with long-term morbidity including chronic renal disease, osteoporosis, cataracts, psychosocial impairment, and importantly, atherosclerotic vascular disease (ASVD). The latter (myocardial infarction, angina, peripheral vascular disease and stroke) are strikingly accelerated, occurring in subjects who are predominantly premenopausal women at an age when ASVD is rare or unusual. Although much is known about the biology, risk factors, and the prevention of atherosclerosis in normal individuals, little work has been done in SLE. In fact, ASVD in people with SLE may be a different disease. Approximately 1 .5% of SLE patients per year will have a myocardial infarction or equivalent; about 0.5% of SLE patients per year will have a stroke. The risk factors for ASVD in SLE are based on small, retrospective, single center studies. These suggest that the risk factors known for the general population (i.e., smoking, obesity, sedentary lifestyle, high LDL cholesterol, etc.) are also observed in SLE. The best study of risk factors shows that even accounting for the known factors, SLE and/or its treatment (glucocorticoids) is by far the most important. Our current management of cardiovascular risk factors in SLE patients with ASVD is substandard and our adherence to national guidelines for prevention is substandard. It is not known whether improving either will prevent these disastrous outcomes. Very little is known about the risk factors in African Americans with SLE, although there is data to suggest that they may not be identical to those seen in Caucasian populations. The study of the best and most effective means to prevent ASVD in SLE and in African Americans with SLE and in African Americans with SLE should be a major priority. (
Rheumatology, 2005
Objective. To determine the relationship between the presence of antiphospholipid (aPL) antibodies, hydroxychloroquine use and the occurrence of thrombotic events in patients with systemic lupus erythematosus (SLE). Methods: Four hundred and forty-two SLE patients from the LUMINA (Lupus in Minorities: Nature vs Nurture) cohort, a multiethnic (Hispanics from Texas, n ¼ 99 and Puerto Rico, n ¼ 36; African Americans, n ¼ 172; and Caucasians, n ¼ 135) cohort, were studied by generalized estimating equation (GEE) to determine the relationship between antiphospholipid (aPL) antibodies (measured as IgG and IgM aPL antibodies and/or the lupus anticoagulant) at enrolment or historically prior to enrolment, hydroxychloroquine use (ever) and the occurrence of thrombotic (central and/or peripheral, arterial and/or venous) events after adjusting for known and possible confounders [socioeconomic-demographic features, smoking, disease activity and damage, serum cholesterol levels, anti-oxidized low-density lipoprotein IgG and IgM antibodies, and high-sensitivity (hs) C-reactive protein]. Postanalysis correlation between aPL and anticardiolipin (aCL) assays was attempted by performing aCL assays on random samples of patients whose aPL status was known. Results. A number of clinical variables were significant in the univariable analyses; however, in the multivariable GEE analyses, only smoking [odds ratio (OR) 2.777, 95% confidence interval (CI) 1.317-5.852] and disease activity as measured by the SLAM (Systemic Lupus Activity Measure) (OR 1.099; 95% CI 1.053-1.147) were significant. In particular, hydroxychloroquine use, which appeared to be protective against thrombotic events in the univariable analyses, was not retained in the multivariable analyses. aPL antibodies were not significant in either analysis. Few additional aPL-positive patients emerged from the validation study.
Risk Factors for Cardiovascular Disease in Systemic Lupus Erythematosus
Circulation, 2001
Background-Cardiovascular disease (CVD) is overrepresented in patients with systemic lupus erythematosus (SLE). We determined the prevalence of traditional and nontraditional risk factors for CVD in SLE patients with and without CVD compared with controls. Methods and Results-Twenty-six women (aged 52Ϯ8.2 years) with SLE and a history of CVD (SLE cases) were compared with 26 age-matched women with SLE but without manifest CVD (SLE controls) and 26 age-matched population-based control women (population controls). Common carotid intima-media thickness (IMT) was measured by B-mode ultrasound as a surrogate measure of atherosclerosis. SLE cases had increased IMT compared with SLE controls (Pϭ0.03) and population controls (Pϭ0.001), whereas IMT of SLE controls did not differ from population controls. SLE cases had raised plasma concentrations of circulating oxidized LDL (OxLDL; Pϭ0.03), as measured by the monoclonal antibody EO6, and autoantibodies to epitopes of OxLDL (PϽ0.001); dyslipidemia with raised triglycerides (PϽ0.001) and lipoprotein(a) (Pϭ0.002) and decreased HDL-cholesterol concentrations (Pϭ0.03); raised ␣-1-antitrypsin (Pϭ0.002), lupus anticoagulant (Pϭ0.007), and homocysteine levels (Pϭ0.03); more frequent osteoporosis (Pϭ0.03); and a higher cumulative prednisolone dose (Pϭ0.05) compared with SLE controls. Disease duration, smoking, blood pressure, body mass index, and diabetes mellitus did not differ significantly between the groups. Conclusions-A set of distinct CVD risk factors separate SLE cases from SLE controls and population controls. If confirmed in a prospective study, they could be used to identify SLE patients at high risk for CVD in order to optimize treatment. (Circulation. 2001;104:1887-1893.)
Preclinical vascular disease in systemic lupus erythematosus and primary antiphospholipid syndrome
Rheumatology, 2005
Objective. To determine the prevalence of preclinical vascular disease and associated risk factors in patients with systemic lupus erythematosus (SLE) or primary antiphospholipid syndrome (APS). Methods. We consecutively studied 70 SLE patients and 25 primary APS patients without clinical coronary artery disease. The control group included 40 healthy women. Carotid ultrasound was performed and the intima-media wall thickness (IMT) and presence of plaque was investigated in all patients and controls. Traditional vascular risk factors and SLE-disease and treatment related factors were also analysed. Results. SLE patients had a higher prevalence of traditional atherosclerosis risk factors: hypertension (P_0.005) and dyslipidaemia (P_0.05) and higher levels of total cholesterol (P^0.03), triglycerides (P^0.004) and apolipoprotein B (P^0.04). The prevalence of carotid plaque was higher and appeared earlier in SLE patients than in the primary APS patients or controls (P_0.001). The IMT was similar in the three groups. SLE patients with secondary APS had a higher prevalence of carotid plaque than patients with primary APS (37.5% vs 8%, P^0.03). The presence of plaque in SLE patients was associated with a higher SLICC score (2.40 AE 1.78 vs 1.02 AE 1.18, P^0.002), higher ECLAM score (3.10 AE 2.32 vs 1.84 AE 1.59, P^0.02) and older age (47.3 AE 8.44 vs 37.38 AE 11.28, P^0.003) at the time of carotid ultrasound study. Conclusion. Plaque prevalence in patients with primary APS is similar to that of controls and inferior to that of SLE patients with secondary APS. SLE patients have a high prevalence of early carotid atherosclerosis that is associated with cumulative disease damage and disease activity.
Lupus science & medicine, 2016
To describe the frequency of myocardial infarction (MI) prior to the diagnosis of systemic lupus erythematosus (SLE) and within the first 2 years of follow-up. Methods: The systemic lupus international collaborating clinics (SLICC) atherosclerosis inception cohort enters patients within 15 months of SLE diagnosis. MIs were reported and attributed on a specialised vascular event form. MIs were confirmed by one or more of the following: abnormal ECG, typical or atypical symptoms with ECG abnormalities and elevated enzymes (≥2 times upper limit of normal), or abnormal stress test, echocardiogram, nuclear scan or angiogram. Descriptive statistics were used. Results: 31 of 1848 patients who entered the cohort had an MI. Of those, 23 patients had an MI prior to SLE diagnosis or within the first 2 years of disease. Of the 23 patients studied, 60.9% were female, 78.3% were Caucasian, 8.7% black, 8.7% Hispanic and 4.3% other. The mean age at SLE diagnosis was 52.5 ±15.0 years. Of the 23 MIs that occurred, 16 MIs occurred at a mean of 6.1±7.0 years prior to diagnosis and 7 occurred within the first 2 years of follow-up. Risk factors associated with early MI in univariate analysis are male sex, Caucasian, older age at diagnosis, hypertension, hypercholesterolaemia, family history of MI and smoking. In multivariate analysis only age (OR=1.06 95% CI 1.03 to 1.09), hypertension (OR=5.01, 95% CI 1.38 to 18.23), hypercholesterolaemia (OR=4.43, 95% CI 1.51 to 12.99) and smoking (OR=7.50, 95% CI 2.38 to 23.57) remained significant risk factors. Conclusions: In some patients with lupus, MI may develop even before the diagnosis of SLE or shortly thereafter, suggesting that there may be a link between autoimmune inflammation and atherosclerosis.
Prevalence of major adverse cardiovascular events among Saudi patients with systemic lupus erythematosus compared with the general population: updates from the national SLE and PURE cohorts, 2024
Objective This study examined the prevalence of major adverse cardiovascular events (MACE) among Saudi patients with SLE and the general population and considered factors associated with such outcomes were taken into consideration. Methods This is a cohort study evaluating the period prevalence of MACE from 2020 to 2023. The study used two datasets, namely the Saudi national prospective cohort for SLE patients and the Prospective Urban-Rural Epidemiology Study Saudi subcohort (PURE-Saudi) for the general population. Participants in both studies were monitored using a standardised protocol. MACE was defined as myocardial infarction (MI), stroke or angina. The analysis was adjusted for demographics, traditional cardiovascular risk factors and SLE diagnosis through logistic regression models. Results The PURE and national SLE cohorts comprised 488 and 746 patients, respectively. Patients with SLE from the SLE cohort were younger (40.7±12.5 vs 49.5±8.6 years) and predominantly female (90.6% vs 41.6%). The prevalence of traditional risk factors was greater in the PURE cohort compared with the SLE cohort. These factors included dyslipidaemia (28.9% vs 49.4%), obesity (63% vs 85%) and diabetes (7.8% vs 27.2%), but not hypertension (19.3% vs 18.8%). MACE (defined as MI or stroke or venous thromboembolism or heart failure) occurred more frequently in patients with SLE (4.3% vs 1.6%, p=0.004). Older age and lupus diagnosis were independently associated with MACE after adjusting for conventional risk factors. The odds of MACE were significantly related to age and lupus diagnosis (p=0.00 and p=0.00, respectively), but not cardiovascular disease (CVD) risk factors (p=0.83). Conclusion Patients with SLE have a significantly higher risk of developing MACE than the general population. This risk is not well explained by traditional risk factors, which may explain the failure of CVD risk scores to stratify patients with SLE adequately. Further studies are needed to understand CVD risk's pathogenesis in SLE and mitigate it.
2008
Atherosclerosis is a chronic inflammatory disorder characterized by immune cell activation, inflammation driven plaque formation and subsequent destabilization. In other disorders of an inflammatory nature, the chronic inflammatory state per se has been linked to acceleration of the atherosclerotic process which is underlined by an increased incidence of cardiovascular disease (CVD) in disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and antiphopholipid (Hughes) syndrome (APS). SLE is an autoimmune disease that may affect any organ. Premature coronary heart disease has emerged as a major cause of morbidity and mortality in SLE. In addition to mortality, cardiovascular morbidity is also markedly increased in these patients, compared with the general population. The increased cardiovascular risk can be explained only partially by an increased prevalence of classical risk factors for cardiovascular disease; it also appears to be related to inflammation. Inflammation is increasingly being considered central to the pathogenesis of atherosclerosis and an important risk factor for vascular disease. Recent epidemiologic and pathogenesis studies have suggested a great deal in common between the pathogenesis of prototypic autoimmune disease such as SLE and that of atherosclerosis.
Rheumatology, 2009
Objective. To determine the features predictive of atherosclerotic cardiovascular damage in patients with SLE. Methods. SLE LUMINA (LUpus in MInorities: NAture vs nurture) patients (n ¼ 637), aged 516 years, disease duration 45 years at baseline (T0), of African-American, Hispanic and Caucasian ethnicity were studied. Atherosclerotic cardiovascular damage was defined by the following items of the SLICC Damage Index (SDI) cardiovascular domain: angina or coronary artery by pass surgery, myocardial infarction and/or congestive heart failure; factors associated with its occurrence were examined by univariable and multivariable regression analyses. Results. Forty-three (6.8%) of 637 patients developed cardiovascular damage over a mean AE S.D. total disease duration of 6.6 AE 3.6 years. Nearly 90% of the patients were women with a mean AE S.D. age of 36.5 (12.6) years; all ethnic groups were represented. By multivariable analyses, after adjusting for the cardiovascular manifestations present, age [odds ratio (OR) ¼ 1.06; 95% CI 1.03, 1.09], male gender (OR ¼ 3.57; 95% CI 1.35, 9.09) SDI at baseline (OR ¼ 1.28; 95% CI 1.09, 1.50) and CRP levels [highest tertile (OR ¼ 2.63; 95% CI 1.17, 5.91)] were associated with the occurrence of cardiovascular damage, whereas the number of years of education was negatively associated with such outcome (OR ¼ 0.85; 95% CI 0.74, 0.94). Conclusions. Our data suggest that atherosclerotic cardiovascular damage in SLE is multifactorial; traditional (age, gender) and diseaserelated factors (CRP levels, SDI at baseline) appear to be important contributors to such an occurrence. Tight control of the inflammatory process must be achieved to prevent it.
The Journal of rheumatology, 2006
We describe the pattern of incidence of thrombovascular events after diagnosis of systemic lupus erythematosus (SLE) in a cohort of lupus patients. Descriptive study of prospectively collected data using incidence rates of thrombovascular events and 95% confidence intervals (CI) calculated for predetermined periods of observation. Kaplan-Meier survival curves were plotted to estimate thrombovascular event-free survival. Among 426 individuals, person-years contributed were as follows: 399 persons and 4356.0 person-years for all events; 417 persons and 4691.9 person-years for arterial events; and 408 persons and 4846.6 person-years for venous events. The incidence of thrombovascular events was highest during the first year after SLE diagnosis (4.00, 95% CI 2.24-6.59) and after 20 years (ranging from 3.32, 95% CI 1.52-6.30, to 4.99, 95% CI 0.60-18.01), and was lowest between 1 and 5 years after SLE diagnosis (1.00, 95% CI 0.53-1.72). A similar pattern was observed for arterial events, ...
Atherosclerosis risk factors in systemic lupus erythematosus
Current Rheumatology Reports, 2009
Cardiovascular disease (CVD) has emerged as a leading cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Growing evidence suggests that infl ammation plays a key role in the pathogenesis of atherosclerosis from initial endothelial dysfunction to rupture of atheromatous plaques. The increased frequency of atherosclerosis in SLE is likely due to a complex interplay among traditional risk factors, disease-related factors such as medications and disease activity, and infl ammatory and immunogenic factors. Identifi cation of these novel risk factors will lead to a better understanding of CVD pathogenesis and may also provide targets for potential treatment strategies. When caring for SLE patients, clinicians should be aware of the increased CVD risk and treat the known modifi able risk factors in addition to controlling disease activity and infl ammation.
Arthritis Care & Research, 2014
Objectives-To investigate risk factors in the subclinical atherosclerosis progression as measured by coronary artery calcium (CAC) and aorta calcium (AC) in women with Systemic Lupus Erythematosus (SLE) (cases) and in comparison with a control population. Methods-A cohort of 149 cases and 124 controls participated in the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Demographic information, cardiovascular and SLE risk factors, and laboratory assessments were collected at an initial visit. CAC and AC were measured by electron beam computed tomography (CT) or multi-detector CT at an initial and a follow-up visit. Logistic regression models were used to identify predictors of progression in CAC and AC; multivariate models were adjusted for age, hypertension, and total cholesterol/HDL ratio. Results-Higher modified ACR/SLICC-DI (OR 2.15, 95%CI 1.33-3.57), use of a corticosteroid (OR 2.93, 95%CI 1.14-7.86), and use of aspirin (OR 4.23, 95%CI 1.53-11.74) were associated with CAC progression in multivariate models. Presence of SLE (OR 2.64, 95%CI 1.26-5.72), lower C3 (OR 0.54, 95%CI 0.33-0.87), lower C4 (OR 0.49, 95% CI 0.27-0.86), use of a corticosteroid (OR 2.73, 95%CI 1.03-7.64), higher corticosteroid dose (OR 1.77, 95%CI 1.12-3.00), higher lipoprotein(a) (OR 1.80, 95%CI 1.11-2.98), higher homocysteine (OR 2.06, 95%CI 1.06-4.29) were associated with AC progression in multivariate models. Conclusions-Higher disease damage at the first study visit, as measured by the modified ACR/ SLICC-DI, may predict increased risk in CAC progression, whereas higher disease activity at the first study visit, as measured by hypocomplementemia and use of corticosteroids, may predict increased risk in AC progression.