scholarly journals THU0269 Electrocardiographic nonspecific ST-T abnormalities are associated with higher modified framingham risk score in systemic lupus erythematosus patients without clinical cardiovascular disease

Author(s):  
E George ◽  
T Perez-Recio ◽  
L Geraldino-Pardilla
2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Panafidina ◽  
T V Popkova ◽  
D S Novikova

Abstract Background Nephritis in systemic lupus erythematosus (SLE) is a factor contributing to early development of atherosclerosis (AS). Objectives The aim of the study is to determine differences in cardiovascular risk factors and AS in SLE pts with and without lupus nephritis (LN). Methods The study included 162 females, age 35 [26–43] years (median [interquartile range 25–75%])) with SLE (ACR,1997). We divided SLE pts on two groups, comparable in age: the 1st group is the pts with LN (n=84, 52%), the 2nd - without LN (n=78, 48%). We considered traditional factors of cardiovascular disease (CVD): (smoking, family history of CVD, blood pressure, cholesterol (total, HDL, LDL) and triglyceride (TG) levels, body mass index, diabetes mellitus) and SLE-related factors (age at onset, duration, clinical features, SLE Disease Activity Index (SLEDAI-2K) and the Systemic Lupus International Collaborating Clinics damage index (SLICC/DI), treatment with steroids); intima-media thickness (IMT) and the 10-year risk for coronary events. Carotid intima-media wall thickness of common carotid arteries was measured by high resolution B-mode ultrasound. The 10-year risk for coronary events was estimated by the Framingham risk equation. Results Median SLE duration was 8,0 [2,3–17,0] years, SLEDAI 2K – 8 [3–16], SLICC/DI score – 2 [0–3], duration of prednisone treatment – 72 [26–141] months. SLE pts from the 1st group had higher prevalence of hypertension (61% vs 36%, p<0,01), systolic blood pressure (130 [110–150] vs 120 [110–130]mm Hg, p<0,01), diastolic blood pressure (80 [70–95] vs 70 [70–80] mm Hg, p<0,05), TG concentration (136 [98–184] vs 100 [61–162] mg/dl, p<0,01), Framingham Risk Score (5 [1–30] vs 1 [1–27]%, p<0,05), SLEDAI-2K (12 [5–19] vs 4 [2–10], p<0,ehz745.08501), SLICC/DI score (2 [0–4] vs 0 [0–2], p<0,01), prednisone therapy duration (95 [26–192] vs 44 [14–98] months, p<0,05), prednisone cumulative dose (34,4 [13,6–82,5] vs 15,7 [6,2–35,2] g, p<0,001), mean IMT (0,73 [0,65–0,83] vs 0,67 [0,61–0,75] mm, p<0,01), than the pts from the 2nd group. There is no difference in CVD frequency in these groups (17% vs 8%, p=0,084). Conclusions SLE patients with and without LN had no difference in frequency of clinical manifestations of AS (CVD), but had a greater value of mean IMT, Framingham Risk Score and a higher incidence of both traditional (hypertension, TG concentration) and SLE-related (disease activity, prednisone therapy) risk factors for AS.


Lupus ◽  
2011 ◽  
Vol 20 (14) ◽  
pp. 1526-1534 ◽  
Author(s):  
VK Kawai ◽  
JF Solus ◽  
A Oeser ◽  
YH Rho ◽  
P Raggi ◽  
...  

Women with systemic lupus erythematosus (SLE) have increased risk for coronary heart disease (CHD) which is underestimated by the Framingham risk score (FRS). We hypothesized that new risk scores that include inflammation or vascular age in the risk calculation would better identify women with SLE at risk for CHD, particularly in those with subclinical coronary atherosclerosis. We calculated the FRS and Reynolds risk score (RRS) in 121 women with SLE and 65 age-matched female controls; coronary age-modified risk scores (camFRS, camRRS) were calculated using coronary age derived from the coronary artery calcium (CAC) score. Risk scores were compared in SLE and controls, and in SLE patients with and without CAC. Although CAC was present in 21 SLE patients (17%) and four controls (6%) ( p = 0.033); the FRS, camFRS, RRS, and camRRS, did not differ significantly among SLE and controls ( p > 0.05), but were all significantly higher in SLE patients with CAC compared with those without ( p < 0.001 for all). The camFRS (8%, p = 0.016) but not camRRS (5%, p = 0.221) assigned significantly more SLE patients to a category of ≥ 10% risk than conventional FRS (1%) and RRS (2%). The RRS was of limited use but coronary age may improve CHD risk prediction in SLE.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Saluja ◽  
H Contractor ◽  
M Daniells ◽  
J Sobolewska ◽  
K Khan ◽  
...  

Abstract Background There is existing evidence to suggest a correlation between coronary artery calcification (CAC) measured using ECG-triggered chest computed tomography and cardiovascular disease. Further evidence has emerged to suggest a correlation between CAC measured using non-gated CT scans and cardiovascular disease. Herein, we sought to ascertain the utility of incidental findings of CAC on non-triggered high resolution CT (HRCT) thorax used for patients undergoing lung cancer screening or follow-up for interstitial lung disease and Framingham risk score (FRS) in predicting cardiovascular events. Methods The Computerised Radiology Information Service (CRIS) database was manually searched to determine all HRCT scans performed in a single trust from 05/2015 to 05/2016. The reports issued by Radiologists and images of selected studies were reviewed. For patients with CAC, we calculated the calcium score for patients using the Agatston method. Clinical events were determined from the electronic medical record without knowledge of patients' CAC findings. For these patients, the Framingham Risk Score (FRS) was also calculated. The primary end point of the study was composite of all-cause mortality and cardiac events (non-fatal myocardial infarction, coronary revascularization, new atrial fibrillation or heart failure episode requiring hospitalization). Results We selected 300 scans from a total of approximately 2000 scans performed over this time. Data at follow up was available for 100% of the patients, with a median duration of follow up of 1.6 years. Moderate to severe CAC was found in 35% of people. Multivariable analysis showed good concordance between CAC and FRS in predicting composite clinical end point. The Odds Ratio for cardiac events in patients with moderate to severe CAC was 5.3 (p&lt;0.01) and for composite clinical end point was 3.4 (p&lt;0.01). This is similar to the OR predicted by the FRS: 4.8; p&lt;0.01 and 3.1; p&lt;0.01 respectively. Only 6.2% of patients with moderate to severe CAC were currently statin treated. Conclusion In this retrospective study of patients with respiratory disease attending for HRCT scanning, co-incidentally detected CAC predicts cardiac events, with good concordance with the FRS. The incidental finding of CAC on non-gated CT scanning should be reported with Agatston score calculation allowing consideration of intervention to mitigate cardiovascular risk and optimize. Further multi-centre prospective studies of this strategy, with a larger patient cohort should be conducted to clarify the utility of CAC as a prediction tool to modify cardiac risk. Funding Acknowledgement Type of funding source: None


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hua-Chen Chan ◽  
Liang-Yin Ke ◽  
Hsiu-Chuan Chan ◽  
Hung Su ◽  
An-Sheng Lee ◽  
...  

Background: Patients with systemic lupus erythematosus (SLE) are twice more likely to develop cardiovascular disease than the general population, even though their plasma LDL cholesterol (LDL-C) levels are usually not elevated. To delineate the mechanisms, we examined the chemical properties of their LDL. Methods and Results: LDL isolated from SLE patients (LDL-C, 105±33 mg/dL; n=24) exhibited greater mobility in agarose gel electrophoresis than LDL of healthy control subjects (LDL-C, 121±25 mg/dL; n=24), secondary to an increased distribution of L5 (2.30±1.3% vs. 0.7±0.3%; P <0.0001), the most electronegative subfraction of LDL identified by anion-exchange chromatography, in total LDL. CX3CL1 is a membrane-bound chemokine expressed in injured endothelial cells (ECs). CD16 + monocytes are CX3CR1-expressing cells that recognize CX3CL1. Compared with control, SLE patients had a twofold ( P <0.001) increase in CX3CL1 and a threefold ( P <0.0001) increase in CD16 + monocytes in the plasma. Moreover, there was a positive correlation between the CX3CL1 and L5 levels (R=0.45; P <0.018). MALDI/TOF mass spectrometry of the lipid extracted from SLE-LDL revealed a shift from phosphatidylcholines (PCs) to lyso-PCs (LPCs), including m/ z 496.33, 524.36, 537.01, 550.94, when compared with the lipid of control LDL (Figure). The shift was especially prominent in L5. Exposing human aortic ECs to L5 but not normal LDL resulted in a fivefold ( P <0.0001) increase in CX3CL1 expression with concomitant apoptosis. These effects of L5 were significantly attenuated by blocking the platelet-activating receptor, confirming the role of phospholipids in L5’s bioactivity. Conclusions: The increased distribution of LPC-rich electronegative LDL, which induces CX3CL1-CX3CR1 interactions between vascular cells, may contribute to the increased cardiovascular disease prevalence in SLE in the absence of LDL-C elevation.


2018 ◽  
Vol 77 (7) ◽  
pp. 1063-1069 ◽  
Author(s):  
Dag Leonard ◽  
Elisabet Svenungsson ◽  
Johanna Dahlqvist ◽  
Andrei Alexsson ◽  
Lisbeth Ärlestig ◽  
...  

ObjectivesPatients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) have increased risk of cardiovascular disease (CVD). We investigated whether single nucleotide polymorphisms (SNPs) at autoimmunity risk loci were associated with CVD in SLE and RA.MethodsPatients with SLE (n=1045) were genotyped using the 200K Immunochip SNP array (Illumina). The allele frequency was compared between patients with and without different manifestations of CVD. Results were replicated in a second SLE cohort (n=1043) and in an RA cohort (n=824). We analysed publicly available genetic data from general population, performed electrophoretic mobility shift assays and measured cytokine levels and occurrence of antiphospholipid antibodies (aPLs).ResultsWe identified two new putative risk loci associated with increased risk for CVD in two SLE populations, which remained after adjustment for traditional CVD risk factors. An IL19 risk allele, rs17581834(T) was associated with stroke/myocardial infarction (MI) in SLE (OR 2.3 (1.5 to 3.4), P=8.5×10−5) and RA (OR 2.8 (1.4 to 5.6), P=3.8×10−3), meta-analysis (OR 2.5 (2.0 to 2.9), P=3.5×10−7), but not in population controls. The IL19 risk allele affected protein binding, and SLE patients with the risk allele had increased levels of plasma-IL10 (P=0.004) and aPL (P=0.01). An SRP54-AS1 risk allele, rs799454(G) was associated with stroke/transient ischaemic attack in SLE (OR 1.7 (1.3 to 2.2), P=2.5×10−5) but not in RA. The SRP54-AS1 risk allele is an expression quantitative trait locus for four genes.ConclusionsThe IL19 risk allele was associated with stroke/MI in SLE and RA, but not in the general population, indicating that shared immune pathways may be involved in the CVD pathogenesis in inflammatory rheumatic diseases.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Meghan Angley ◽  
Tene T Lewis ◽  
Penelope P Howards ◽  
Sung Lim

Background: Patients diagnosed with systemic lupus erythematosus (SLE) are at greater risk of cardiovascular disease (CVD) and death at earlier ages than the general population, with African Americans (AA) at risk at earlier ages than non-AAs. However, the association between race and recurrent hospitalizations for CVD, which are associated with mortality, has not been explored. Methods: The Georgia Lupus Registry (GLR) is a population-based registry of individuals with SLE in 2002-2004 in Atlanta, Georgia. Both incident and prevalent cases were enrolled, and we included all cases diagnosed beginning in 2000. The GLR was matched to Georgia inpatient hospital discharge records from 2000-2013. Using ICD-9-CM codes, we identified hospitalizations classified as having coronary heart disease, peripheral artery disease, cerebrovascular disease or heart failure. The Prentice-Williams-Peterson Model with a total time scale measured from diagnosis was used to examine recurrent time to event data. We truncated the number of hospitalizations at 3 to maintain stable modeling estimates. Patients were censored at the time of death or at the end of 2013. Models were adjusted for sex and age at diagnosis. Results: A total of 556 participants in the GLR (87% female, 73% AA) had a median age at SLE diagnosis of 38 years and 27% experienced at least 1 CVD hospitalization, while 17% experienced ≥ 2. Overall, AA race was associated with recurrent hospitalizations (adjusted hazard ratio [aHR]: 1.7, 95% confidence interval [CI]: 1.2, 2.3). In an event-specific stratified analysis, the association between AA race and the hazard of recurrence became even more pronounced in later events (Event 1 aHR: 1.2, 95% CI: 1.0, 1.5; Event 2 aHR: 1.5, 95% CI: 1.2, 2.2; Event 3 aHR: 1.9, 95% CI: 1.1, 3.2). Conclusions: African-Americans with SLE were more likely to experience recurrent hospitalizations for CVD than their non-AA counterparts, suggesting that AA individuals with SLE may be more vulnerable to CV complications of SLE. Figure 1. Survival curve for 1st event


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