Risk factors and early detection of atherosclerosis in rheumatoid arthritis

Groot, Lodewijk de; Posthumus, Marcel D.; Kallenberg, Cees G. M.; Bijl, Marc

doi:10.1111/j.1365-2362.2010.02333.x

Cited by 37 publications

(28 citation statements)

References 46 publications

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“…Disease activity has been related to an increased risk for subclinical atherosclerosis and cardiovascular events in adult CID patients (30). Corticosteroids treatment has also been associated with increased subclinical atherosclerosis in adults with CID (31).…”

Section: Discussionmentioning

confidence: 99%

Changes in vascular function and structure in juvenile idiopathic arthritis

Vlahos¹,

Theocharis²,

Bechlioulis³

et al. 2011

Arthritis Care & Research

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Objective. Chronic inflammatory diseases in adults have been associated with increased cardiovascular risk and impaired vascular function. We aimed to assess the presence of early vascular dysfunction in patients with juvenile idiopathic arthritis (JIA) and investigate the role of inherent inflammatory process of JIA in vascular health. Methods. Thirty patients with JIA (age range 7-18 years) were compared to 33 age-and sex-matched controls. Endothelial function (brachial artery flow-mediated dilation [FMD]), carotid intima-media thickness (IMT), and arterial stiffness were examined. Endothelial inflammation was assessed by intercellular adhesion molecule 1 (ICAM-1) and P-selectin measurements. Results. Patients with JIA showed decreased FMD compared to controls (P ‫؍‬ 0.001), independent of age (P ‫؍‬ 0.9 among age subgroups). Baseline differences in erythrocyte sedimentation rate, ICAM-1, and glucose between the 2 groups accounted for the difference in FMD. The presence of systemic JIA was associated with greater IMT compared to patients with oligoarticular disease, polyarticular disease, or controls (P ‫؍‬ 0.014, P ‫؍‬ 0.069, and P ‫؍‬ 0.046, respectively). The difference in IMT between systemic versus oligoarticular/polyarticular JIA was attributed to the following risk factors: age, body mass index, blood pressure, disease activity, and corticosteroids use. There were no differences in arterial stiffness indices between JIA patients and controls or between patients with systemic versus nonsystemic disease. Conclusion. Endothelial function is impaired in patients with JIA at a very young age, while IMT is increased only in the presence of systemic JIA. Vascular dysfunction may be partly attributed to the effects of disease-related characteristics (inflammation, disease activity, and medications).

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Section: Discussionmentioning

confidence: 99%

Changes in vascular function and structure in juvenile idiopathic arthritis

Vlahos¹,

Theocharis²,

Bechlioulis³

et al. 2011

Arthritis Care & Research

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“…The severity of inflammatory activity predicts CV events and mortality in RA patients [6,18,19]. Certain medications used to treat IA and SLE may also contribute to the increased risk of CVD, including nonsteroidal anti-inflammatory drugs (NSAIDs) [20], COX-2 inhibitors [5,20], steroids [21,22], and anti-folate medications such as methotrexate [23,24].…”

Section: Introductionmentioning

confidence: 99%

Lack of cardiovascular risk assessment in inflammatory arthritis and systemic lupus erythematosus patients at a tertiary care center

2011

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The purpose of this study is to evaluate cardiovascular risk assessment at a Canadian rheumatology center and describe the cardiovascular risk of inflammatory arthritis (IA) and systemic lupus erythematosus (SLE) patients using the Framingham risk score. A retrospective chart review of 504 patients attending nine rheumatology practices at the University of Alberta Hospital was performed. A pre-specified case report form detailed patient demographics, cardiac risk factors, variables for the Framingham 2008 score, disease activity, and medication use. In this group of 504 patients, 64 (12.7%) had SLE (male (M) to female (F) ratio=60:4) and 440 (87.3%) had an IA (M to F ratio=117:323). Of the SLE patients, 31 (48.4%) met four or more American College of Rheumatology (ACR) criteria, 33 (51.6%) had less than four ACR criteria. Of the IA patients, 156 (35.5%) were CCP positive and 257 (58.4%) were RF positive. Utilizing the chart data, retrospective Framingham risk scores were calculable for one (1.6%) SLE patient and three (0.68%) IA patients. The most common cardiac risk factors not documented in the medical records of both the SLE and IA patients included: (1) positive family history of MI, (2) diabetes, and (3) lipid status. The blood pressure was more frequently documented in the SLE patients (93.8%) compared to the IA patients (56.1%). While traditional cardiac risk factors only partially contribute to the increased cardiovascular risk in these patients, cardiovascular risk assessment was suboptimally performed amongst a large group of rheumatologists. A dedicated cardiovascular risk reduction clinic for inflammatory rheumatic diseases has been established at this site to fulfill this need and evaluate treatment strategies.

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“…A recently identified new player in atherosclerosis pathogenesis is the macrophage migration inhibitory factor (MIF) which induces the pro-inflammatory mediators TNF-, IL-1, IL-6 and metalloproteinases (MMPs), activates T cells and promotes angiogenesis. In mice with advanced atherosclerosis, MIF blockade led to plaque regression and reduced monocyte and T-cell content in the plaques (de Groot, Posthumus et al 2010). The increased arterial stiffness found in RA patients is significantly correlated with disease duration and inflammatory markers such as CRP and IL-6 (Tabas, Williams et al 2007).…”

Section: Ramentioning

confidence: 96%

“…Pro-inflammatory cytokines such as TNF-and IL-6 are released into the systemic circulation and have multiple effects on distant organs including the endothelium and the formation of the atherosclerotic plaque through upregulation of adhesion molecules such as vascular cellular adhesion molecule (VCAM), inhibiting of endothelial nitric oxide (eNOS) production and induction of formation of oxidized LDL (de Groot, Posthumus et al 2010). Blockade of TNF-in RA reduces cytokine levels, leucocyte trafficking and platelet levels which may all promote atherosclerotic complications (Full, Ruisanchez et al 2009).…”

Section: Ramentioning

confidence: 99%

“…As the atherosclerotic plaque matures, the apoptosis of cells in the plaque leads to extracellular lipid accumulation and cellular debris formation. Under the influence of macrophage proteinases, the fibrous cap of the plaques weakens, ruptures and secondary thrombosis may occur (de Groot, Posthumus et al 2010). In RA patients, genetic regulation of inflammation seems to be implicated in pathogenesis of accelerated atherosclerosis.…”

Section: Ramentioning

confidence: 99%

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