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Featured researches published by A.M. van Sijl.


The Journal of Rheumatology | 2012

Different Type of Carotid Arterial Wall Remodeling in Rheumatoid Arthritis Compared with Healthy Subjects: A Case-Control Study

A.M. van Sijl; K. van den Hurk; M J L Peters; V. P. Van Halm; G. Nijpels; C. D. A. Stehouwer; Yvo M. Smulders; A E Voskuyl; J. M. Dekker; M.T. Nurmohamed

Objective. Rheumatoid arthritis (RA) is associated with an increased cardiovascular (CV) risk, but mechanisms behind this increased risk have not been fully elucidated. Carotid arterial remodeling is the change of structural properties in response to hemodynamic or metabolic factors aimed at keeping wall stress within certain limits. This process might become maladaptive when stress on the arterial wall increases beyond these limits. We investigated whether maladaptive carotid arterial remodeling is present in RA compared with control subjects. Methods. The 2 cohorts were 96 patients with RA and 274 healthy subjects, who were investigated cross-sectionally. Carotid intima-media thickness (cIMT) and interadventitial diameter (IAD) were assessed by B-mode carotid ultrasonography. Lumen diameter (LD), circumferential wall stress (CWS), and circumferential wall tension (CWT) were calculated. Linear regression analyses were used to investigate the association between presence of RA and carotid arterial remodeling. Results. Compared with healthy subjects, RA was associated with a 0.40 mm (9.3%) greater LD, 0.41 mm (7.8%) greater IAD, 10% higher CWS, and 8% higher CWT. The groups had comparable cIMT. Associations remained similar after exclusion of patients with prior CV disease and after adjustment for demographic factors and CV risk factors. Conclusion. RA is associated with maladaptive outward carotid arterial remodeling. These results are relevant because maladaptive outward remodeling is associated with plaque instability and rupture. These results indicate an alternative pathway, beyond the traditional CV risk factors, in RA that amplifies the CV risk.


Annals of the Rheumatic Diseases | 2012

Dyslipidaemia in patients with seropositive arthralgia predicts the development of arthritis

L. A. van de Stadt; A.M. van Sijl; D. van Schaardenburg; M.T. Nurmohamed

Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with cardiovascular disease.1 There are conflicting data as to whether or not this increased risk of cardiovascular disease is already present before the clinical onset of RA.2 In active RA an unfavourable lipid profile is present and is associated with inflammation.3 Patients with arthralgia positive for rheumatoid factor (RF) and/or anticyclic citrullinated peptide antibodies (aCCP) (seropositive) are at risk of developing RA and can be considered as patients with symptoms and systemic autoimmunity associated with RA without clinical arthritis.4 ,5 Considering the close relationship between inflammation and serum lipid levels, we investigated whether an unfavourable lipid profile was associated with the development of RA in patients with seropositive arthralgia. Total cholesterol (TC), high-density lipoprotein cholesterol (HDLc), low-density …


Annals of the Rheumatic Diseases | 2014

A1.77 Interferon regulatory factor 5 (IRF5) gene variant RS2004640 is associated with carotid intima media thickness in rheumatoid arthritis patients

Saskia Vosslamber; A.M. van Sijl; C L Bos; Joyce Lübbers; S de Ridder; A E Voskuyl; M.T. Nurmohamed; Cornelis L. Verweij

Background and Objectives Rheumatoid arthritis (RA) is a chronic inflammatory joint disease and is associated with an increased cardiovascular (CV) risk. Interferons (IFNs), especially IFNβ, might play a role in atherosclerosis as they are known inhibitors of vascular smooth muscle cell proliferation and intimal hyperplasia. We studied whether functional relevant SNPs in the interferon regulatory factor 5 (IRF5) gene are associated with carotid intima media thickness (cIMT), a surrogate maker for CV disease. Materials and Methods In 353 RA patients of the CARRÉ study, IRF5 SNPs rs2004640 and rs4728142 were determined using Taqman Genotyping assay. cIMT was determined in a subgroup of 101 patients by B-mode ultrasonography. Linear regression analyses were used to investigate the association between cIMT and IRF5 genotypes, adjusting for demographic and cardiovascular risk factors. Results Patients homozygous for rs2004640 G-allele have higher cIMT compared to those homozygote for the T-allele (p = 0.019) and a trend towards a higher cIMT was observed (p = 0.103) for patients homozygous for the rs4728142 G-allele versus patients with the AA-genotype. Age was an effect-modifier for this association. Linear regression analysis in patients older than 60 years showed that the rs2004640 GG-genotype was associated with higher cIMT (regression coefficient 0.107 (C. I. 0.008; 0.205), p = 0.035) compared to the TT-genotype. This remained significant after adjustment for traditional risk factors (regression coefficient 0.111 (C. I.0.02; 0.202), p = 0.020). Conclusion We demonstrate that the IRF5 gene variant rs2004640 is associated with preclinical atherosclerosis in RA patients, independent of traditional cardiovascular risk factors. These results might implicate a role for type I IFN in modulating CV disease features in RA.


Annals of the Rheumatic Diseases | 2015

THU0228 Reduction of Inflammation Drives Lipid Changes in Ankylosing Spondylitis

S.C. Heslinga; M J L Peters; M. ter Wee; A.M. van Sijl; Yvo M. Smulders; I. E. van der Horst-Bruinsma; M.T. Nurmohamed

Background In inflammatory diseases, including ankylosing spondylitis (AS), systemic inflammation induces secondary dyslipidaemia with lower total cholesterol (TC) and lower high density cholesterol (HDL-C) levels. Effective anti-inflammatory treatment with tumor necrosis factor (TNF) alpha-blocking therapy has been shown to increase lipid levels, which as a result, may affect cardiovascular (CV) risk. It is still unclear whether lipid changes following TNF-alpha blocking therapy are due to suppressed inflammation, or due to a specific effect of TNF-alpha blocking therapy. Objectives We investigated the effects of changing inflammation levels during treatment with TNF-alpha blocking therapy on the lipid profile in AS patients. Methods 230 consecutive AS patients with an indication for TNF-alpha blocking therapy with etanercept or adalimumab were enrolled. Data was collected at baseline and after 52 weeks of treatment. Serum C-reactive protein (CRP) was measured at each visit. High inflammatory status was defined as CRP≥10mg/L. Non-fasting lipid samples were collected at baseline and at 52 weeks. Results CRP decreased significantly during treatment from 8 (3-22) to 2 (1-6) mg/l (p<0.01). TC, HDL-C and low density lipoprotein cholesterol (LDL-C) increased significantly with 4.6%, 3.7%, and 4.3% respectively. Apolipoprotein A-1 increased with 5.3%, while apolipoprotein B did not change. The TC/HDL-C ratio was not significantly changed after 52 weeks of TNF-alpha blocking therapy. Regression analyses yielded an inverse association between changes in CRP and changes in TC (+0.104 mmol/l per 10mg/l reduction in CRP) and HDL-C (+0.024mmol/l per 10mg/l reduction in CRP) but not TC/HDL-C ratio. Significant changes in TC (+8.2%) and HDL-C (+8.3%) levels were only seen in patients whom CRP levels decreased during treatment from ≥10 mmol/l to <10mmol/l, but again, the TC/HDL-C ratio did not change. Conclusions TNF-alpha blocking therapy is associated with a modest, but broadly parallel increase in TC, LDL-C, and HDL-C that might affect CV risk. Also, our data show, for the first time, that lipid changes following TNF-alpha blocking therapy are mostly due to suppressing inflammation and not to a specific TNF-alpha blocking therapy effect. Finally, consistent with previous findings, our data illustrate that the TC/HDL-C ratio is not appreciably altered by TNF-alpha blocking therapy and is therefore currently the most appropriate marker to determine CV risk in patients with an inflammatory condition. Disclosure of Interest None declared


Annals of the Rheumatic Diseases | 2015

SAT0131 Uric Acid is Associated with Metabolic Syndrome in Longstanding Rheumatoid Arthritis

R. Agca; A.M. van Sijl; Alexandre E. Voskuyl; M.T. Nurmohamed

Background Cardiovascular (CV) risk is enhanced in patients with rheumatoid arthritis (RA). Metabolic syndrome, a cluster of several classic CV risk factors, has been shown to be more prevalent in patients with RA. Previous studies have associated metabolic syndrome with hyperuricemia, a potential marker for cardiovascular morbidity and mortality. Objectives To investigate the relationship between uric acid and metabolic syndrome in a prospective observational cohort of longstanding RA patients. Methods Uric acid was measured in baseline samples of 353 RA patients participating in an ongoing prospective cohort study to assess cardiovascular morbidity and mortality (CARRΈ study). Metabolic syndrome was defined according to the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III, ATP III) (1). Results 23.8% of the patient in this cohort fulfilled the criteria of metabolic syndrome according to the NCEP ATP III guidelines (1). Patients were predominantly females (65.7%) with a mean age of 63±6 years and a mean RA duration of 8±4 years. Elevated uric acid levels in serum were significantly associated with metabolic syndrome in a univariate analysis (table 1). After correction for gender, age, CVD prevalence, RA duration and disease activity in a multivariable model, uric acid remained significantly associated with metabolic syndrome (table 1). Table 1. Logistic regression analysis OR 95% CI P-value Model 1 Metabolic syndrome plus uric acid 2,39 1.33–4.32 0.004 Model 2 Model 1, corrected for age and gender 2,42 1.32–4.42 0.004 Model 3 Model 2, corrected for CVD prevalence 2.55 1.38–4.71 0.003 Model 4 Model 3, corrected for RA duration and disease activity* 2.51 1.34–4.70 0.004* Disease activity was measured with the Disease Activity Score (DAS28). Conclusions Elevated serum uric acid levels were significantly associated with metabolic syndrome in patients with longstanding RA. References Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106(25):3143-3421. Disclosure of Interest None declared


Annals of the Rheumatic Diseases | 2013

THU0044 Different type of carotid arterial wall remodeling in rheumatoid arthritis as compared to healthy subjects

A.M. van Sijl; K. van den Hurk; M J L Peters; V P van Halm; Giel Nijpels; Coen D. A. Stehouwer; Yvo M. Smulders; A E Voskuyl; Jacqueline M. Dekker; M.T. Nurmohamed

Background Rheumatoid arthritis (RA) is associated with an increased cardiovascular (CV) risk, but mechanisms explaining this increased risk have not been fully elucidated. Arteries react on hemodynamic changes by arterial remodeling. Objectives We investigated whether arterial remodeling is different in RA as compared to control subjects. Methods 96 RA-patients and 274 healthy subjects were investigated cross-sectionally in two cohorts. B-mode carotid ultrasonography was used to investigate arterial wall parameters, including carotid intima-media thickness (cIMT), inter-adventitial diameter (IAD) and lumen diameter (LD), calculated as IAD – (2 × cIMT). Using linear regression, the association between presence of RA and arterial wall parameters was assessed. Results RA was associated with a 0.57 mm (9.3%) greater LD. IAD was 0.61 mm (7.8%) higher in RA. cIMT did not differ between RA patients and healthy subjects, resulting in a 4.4% greater wall-to-lumen ratio (ratio of IAD to cIMT, an indicator of outward remodeling) in RA. Associations remained similar after exclusion of patients with prior CV disease and after adjustment for demographic factors and CV risk factors. In RA, disability index and current use of prednisone were significantly associated with a greater wall-to-lumen ratio. Conclusions RA is associated with outward arterial remodelling, which is relevant because this is associated with plaque instability and rupture. Disclosure of Interest None Declared


Annals of the Rheumatic Diseases | 2013

FRI0100 Sustained development of cardiovascular disease in rheumatoid arthritis despite cardioprotective treatment: The 7-year prospective carre-study

A.M. van Sijl; I.A. van den Oever; M J L Peters; V P van Halm; Yvo M. Smulders; Alexandre E. Voskuyl; M.T. Nurmohamed

Background Rheumatoid arthritis (RA) is a chronic inflammatory joint disease which is associated with an increased cardiovascular (CV) risk. Still unknown is whether CV risk factors or the underlying inflammatory process in RA renders these patients more at risk of CV disease (CVD). An increment in these factors over several years might explain this predisposition. Objectives The present study compared changes in these factors over time in RA-patients who did and did not develop CVD during follow-up. Methods 7-year incidence rate of CVD was determined in a prospective cohort of 353 RA-patients. CV risk factors, RA-related factors and medication use were assessed at baseline, at 3-years and at 7-years of follow-up. Associations between the changes in investigated factors and development of CVD were assessed using generalized estimating equation (GEE) analyses. Results After 7 years, there were 62 events over 2361 patientyears of follow-up, incidence rate (IR) of 26.3/1.000 patientyears. This was similar to the IR after 3-years of follow-up. GEE analyses showed that, during follow-up, changes in disease activity score of 28 joints (DAS28) and overall 10-year CV risk estimation (as calculated by SCORE) were associated with incident CVD. Use of biologics increased significantly in patients who did not develop incident CVD vs. those who did (26% vs. 6%), while use of statins increased significantly in patients who did develop incident CVD vs. those who did not (43% vs. 14%). Conclusions An increased risk of incident CVD persists in patients with RA. Changes in both DAS-28 as well as 10-year CV risk estimation (SCORE) were associated with the 7-year CVD incidence. Cardioprotective treatment did not seem to extenuate this association. A more aggressive cardioprotective and anti-inflammatory treatment of RA might mitigate the burden of CVD in RA. Disclosure of Interest None Declared


Annals of the Rheumatic Diseases | 2013

THU0045 Score and framingham predict cv disease incidence in RA patients better than intima-media thickness

A.M. van Sijl; I.A. van den Oever; Hennie G. Raterman; M J L Peters; V P van Halm; Maarten Boers; Yvo M. Smulders; Alexandre E. Voskuyl; M.T. Nurmohamed

Background Rheumatoid arthritis (RA) is a chronic inflammatory disease with an increased cardiovascular (CV) risk. Carotid intima-media thickness (cIMT) predicts CV events in the general population, and hence, is used as a non-invasive screening tool to identify patients at high CV risk. In RA, it is still unclear whether estimated 10-year CV risk models, such as the Systematic Coronary Risk Evaluation (SCORE) and Framingham accurately predict CV disease incidence or whether cIMT measurement can equally predict CV disease incidence. Objectives To investigate the predictive value of SCORE- and Framingham risk models and cIMT for future CV events in RA. Methods CARRΈ is an ongoing cohort study of CV disease in RA. In a subpopulation (n=141) we measured cIMT at baseline; Of those, 120 had no prior CV disease and 10-year risk of fatal and nonfatal CV disease was calculated. We compared these calculations with actual CV events recorded in a mean follow-up of 9 years. During this time, IMT was measured three times. Univariate logistic regression analyses (with standardized odds ratios) investigated the extent to which individual CV risk factors, SCORE, Framingham and cIMT predicted CV disease incidence. Results Thirteen RA patients (incidence rate: 13.5%, 95% confidence interval (CI): 7.8-23.2) developed a CV event, of which four of these events were fatal (incidence rate: 4.2%, 95%>CI: 1.6-11.1). SCORE- and Framingham predictions were very close to actual CV mortality and morbidity and significantly predicted (fatal) CV events. cIMT also showed a trend in prediction of CV disease. cIMT progressed with an annual rate of 0.005mm. Table 1. Logistic regression of CV disease incidence with CV risk factors, IMT and CV risk models Standardized OR (95% CI) p Age 1.80 (1.00-3.23)* 0.048 Systolic blood pressure 1.64 (0.94-2.86) 0.08 Atherogenic index 1.79 (1.06-3.01)* 0.03 cIMT 1.67 (0.97-2.85) 0.06 3-yearly IMT progression 1.19 (0.71-1.99) 0.52 7-yearly IMT progression 1.13 (0.50-2.55) 0.77 10-year Framingham CV-risk 1.82 (1.12-2.96)* 0.02 10-year SCORE CV-risk 1.83 (1.17-2.88)* 0.009 *Significant association between investigated variables and CV disease incidence (p≤0.05). Conclusions This long term follow up study underscores the value of SCORE and Framingham in prediction of CV disease incidence, also in RA. In this study of RA patients the evidence for cIMT, a surrogate marker of CV disease in the general population, had no predictive value. Disclosure of Interest None Declared


Annals of the Rheumatic Diseases | 2013

FRI0142 TNF-blocking therapy reduces cardiovascular disease and risk factors in rheumatoid arthritis:

A.M. van Sijl; I.M. Visman; M J L Peters; C. van Dongen; Yvo M. Smulders; Alexandre E. Voskuyl; M.T. Nurmohamed

Background Patients with rheumatoid arthritis (RA) are at increased risk of cardiovascular (CV) disease. The contribution of inflammation to this increased risk is well recognised. Recent register based studies indicate that suppression of tumour necrosis factor (TNF) lowers CV risk. No register to date has accurately assessed both CV- and RA-related parameters. Methods The CARRΈ study is a Dutch prospective cohort study of 353 randomly selected RA patients, aged 50-75, with 1381 patient years. The Biologics cohort is an ongoing study of 449 Dutch RA patients, also aged 50-75, with 1201 patient years of follow-up since their allocation to their first TNF-blocking agents adalimumab or etanercept. Fatal and non-fatal CV events (according to the international classification of disease, ICD-9) were documented in both cohorts. Cox-proportional hazard analyses were used to investigate the association between use of TNF-blocking agents and CV disease incidence. Results Incidence rate ratio of CV events in RA patients with TNF-blocking therapy versus those without TNF-blocking therapy was: 0.36 (95%>confidence interval (CI): 0.18-0.73), incidence rate: 8.3 vs. 23.2 per 1.000 patient years, respectively. Age- and gender adjusted hazard ratio for CV disease incidence: 0.54 (95%>CI: 0.24-1.21) in favour of patients receiving TNF-blocking therapy, although not statistically significantly so. The magnitude of this association remained stable after additional adjustment for CV risk factors, RA-related parameters and concomitant medication use. There was a difference in baseline characteristics between populations and there was no increase in CV risk factors over time in either group. Patients receiving TNF-blocking therapy, as expected, had a substantial improvement in RA-related parameters over time. Table 1. Incidence of cardiovascular risk factors and cardiovascular events Biologicals cohort (n=442) CARRΈ study (n=283) IRR (95%>CI) Cases IR (95%>CI)/1000 Cases IR (95%>CI)/1000 patientyears patientyears All CV events 9 7.5 (3.9-14.4) 32 23.2 (16.4-32.8) 0.3 (0.1-0.6)* CV mortality 0 0.0 (0.0-0.0) 3 2.2 (0.7-6.7) – CAD 3 2.5 (0.8-7.8) 18 13.0 (8.2-20.7) 0.2 (0.1-0.7) * CVD 6 5.0 (2.3-11.1) 8 5.8 (2.9-16.8) 0.9 (0.3-2.5) PAD 0 0.0 (0.0-0.0) 3 2.2 (0.7-6.7) – CAD, coronary artery disease; CI, confidence interval; CV, cardiovascular; CVD, cerebrovascular disease; IR(R), incidence rate (ratio); PAD, peripheral arterial disease. Conclusions Our observations confirm the association between strong suppression of inflammation and curbing the CV risk in RA. Surprisingly, this CV risk appeared to be independent of CV risk factors. However, whether the reduced incidence of CV disease is due to allocation of patients with certain disease characteristics (more favourable CV risk profile in patients receiving TNF-blocking therapy) is not yet clear and may indicate channelling bias. Disclosure of Interest None Declared


Current Medicinal Chemistry | 2015

Tumor Necrosis Factor Blocking Therapy and Congestive Heart Failure in Patients with Inflammatory Rheumatic Disorders: A Systematic Review

S.C. Heslinga; A.M. van Sijl; K. De Boer; V P van Halm; M.T. Nurmohamed

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M.T. Nurmohamed

VU University Medical Center

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Yvo M. Smulders

VU University Medical Center

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M J L Peters

VU University Medical Center

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Alexandre E. Voskuyl

VU University Medical Center

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V P van Halm

VU University Medical Center

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A E Voskuyl

Vanderbilt University Medical Center

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D. van Schaardenburg

VU University Medical Center

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I.A. van den Oever

VU University Medical Center

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K. van den Hurk

VU University Medical Center

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