Increased arterial stiffness and indication of endothelial dysfunction in long‐standing rheumatoid arthritis

Wållberg‐Jonsson, Solveig; Caidahl, Kenneth; Klintland, Natalia; Nyberg, G.; Rantapää‐Dahlqvist, Solbritt

doi:10.1080/03009740701633238

Cited by 82 publications

(71 citation statements)

References 14 publications

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“…* p < 0.05: AIA + saline vs. control, AIA + Ang-(1-7) vs. AIA + saline. terial stiffness and elevation of vascular resistance due to endothelial dysfunction and inflammation induced by AIA [26] .…”

Section: Discussionmentioning

confidence: 99%

Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis

et al. 2016

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Altered vascular reactivity due to endothelial dysfunction, consequent to vascular damage, is observed in rheumatoid arthritis. We investigated the effect of angiotensin (Ang)-(1-7) on vasculature changes in arthritis induced by complete Freund's adjuvant in male Wistar rats. Arthritis decreased soluble receptor for advanced glycation end products (sRAGE) whereas elevated aortic RAGE expression, increased interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), systolic blood pressure and the contractility induced by phenylephrine and KCl. Moreover, arthritis decreased the relaxing effect of acetylcholine. Neither arthritis nor Ang-(1-7) altered sodium nitroprusside relaxation. Ang-(1-7) reversed the effect of arthritis on TNF-α, sRAGE and RAGE expression without any effect on the IL-1β. Ang-(1-7) decreased phenylephrine and KCl contractility, especially in the endothelial-denuded aorta, whereas increased acetylcholine relaxation in the endothelial-intact aorta. Ang-(1-7) could find its place in the treatment protocol of arthritis and vascular diseases.

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Section: Discussionmentioning

confidence: 99%

Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis

et al. 2016

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“…Although the factors responsible for increased AS are poorly understood, they probably include alterations in structural components of the arterial wall such as elastin and collagen or changes in regulation of muscle tone mediated by vasoactive substances such as endothelial-derived nitric oxide [24,25]. An additional factor that may also promote AS through endothelial dysfunction is acute or chronic inflammation [26]. We do not know the cause of altered aortic elastic properties in patients with fluorosis.…”

Section: Discussionmentioning

confidence: 99%

Aortic Elasticity is Impaired in Patients with Endemic Fluorosis

Varol

Akçay

Ersoy

et al. 2009

Biol Trace Elem Res

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Sixty-three patients with endemic fluorosis (36 males/27 females; mean age 33.9 +/- 8.6 years) and 45 age-, sex-, and body mass index-matched healthy controls (30 males/15 females; mean age 32.7 +/- 8.8 years) were included in this study. Aortic stiffness indices, aortic strain (AS), aortic distensibility (AD), and aortic strain index (ASI) were calculated from the aortic diameters measured by echocardiography and blood pressure obtained by sphygmomanometry. The urine fluoride levels of fluorosis patients were significantly higher than control subjects as expected (1.9 +/- 0.1 mg/l vs. 0.4 +/- 0.1 mg/l, respectively; P < 0.001). AS and AD were significantly lower in fluorosis patients than in the controls (for AS 5.3 +/- 3.6 vs. 8.0 +/- 3.4%; P < 0.001 and for AD 0.2 +/- 0.1 vs. 0.3 +/- 0.1 cm(2) dyn(-1) 10(-3); P < 0.001, respectively). In contrast, significantly higher ASI was observed in fluorosis patients than in the controls (3.4 +/- 0.6 vs. 3.0 +/- 0.4; P < 0.001, respectively). The results of our study demonstrate that elastic properties of ascending aorta are impaired in patients with endemic fluorosis.

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“…in response to immunization) and low-grade chronic systemic inflammation (detected using high sensitivity CRP assays) in healthy individuals has been directly linked with arterial stiffness and vascular dysfunction [32,33]. However, despite this biologically plausible link between inflammation and vascular dysfunction, there are still some controversies and inconsistent results in RA [34,35], where some studies report a lack of association between systemic inflammatory load and endothelial function [36][37][38]. This may be attributed to different methodological approaches (e.g.…”

Section: Inflammation and Endothelial Dysfunc-tionmentioning

confidence: 99%

Vascular Function and Inflammation in Rheumatoid Arthritis: the Role of Physical Activity

Metsios¹,

Kalinoglou²,

Sandoo³

et al. 2010

TOCMJ

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Inflammation disturbs biochemical pathways involved in homeostasis of the endothelium. Research has established clear links between inflammatory mediators, particularly C-reactive protein and tumour necrosis factor alpha, endothelial dysfunction, and atherosclerosis. Endothelial dysfunction and atherosclerosis may be subclinical at early stages, and thus the ability to detect them with non-invasive techniques is crucially important, particularly in populations at increased risk for cardiovascular disease, such as those with rheumatoid arthritis. This may allow the identification of interventions that may reverse these processes early on. One of the best non-pharmacological interventions that may achieve this is physical activity. This review explores the associations between inflammation, endothelial dysfunction, and atherosclerosis and discusses the role of exercise in blocking specific pathways in the inflammation, endothelial dysfunction -atherosclerosis network.

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Increased arterial stiffness and indication of endothelial dysfunction in long‐standing rheumatoid arthritis

Abstract: Arterial stiffness was increased in RA patients. Endothelial dysfunction was implicated and correlated with levels of soluble adhesion molecules. Small vessel resistance correlated with the long-standing inflammatory load in RA.

Cited by 82 publications

References 14 publications

Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis

Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis

Aortic Elasticity is Impaired in Patients with Endemic Fluorosis

Vascular Function and Inflammation in Rheumatoid Arthritis: the Role of Physical Activity

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