Explaining how "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis.

By N. Sattar, D. Mccarey, H. Capell, I. McInnes. Circulation, 2003

986 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/414a57fc65797c26cbef0b0f24a4dbd69cfd0bdc

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In Epidemiology

In Rheumatology

Citations in the corpus

2016 European Guidelines on cardiovascular disease prevention in clinical practice (2017, positive): “There is now clear evidence implicating high-grade inflammation as a pathway for accelerated vascular disease [178].”
2016 European Guidelines on cardiovascular disease prevention in clinical practice (2016, background): “appears to enhance CV risk directly and indirectly via accentuation of existing risk pathways.(178) While early small studies suggested RA increases CV risk beyond other risk markers, the recent analysis of”
Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti–tumor necrosis factor α therapy: Results from the British Society for Rheumatology Biologics Register (2007, background): “Proinflammatory cytokines, including TNF , are involved in modification of lipid profile and insulin resistance (14) and the initiation and progression of atherosclerosis (15,16), hemostasis (17), and atherosclerotic plaque rupture, the most common event leading to an acute MI (15).”
Inflammation, stress, and diabetes. (2005, neutral): “Rheumatoid arthritis also predisposes patients to diabetes and particularly cardiovascular disease, and some evidence indicates a link between inflammatory lung diseases and risk of cardiovascu - lar disease and diabetes (97–99).”
2016 European Guidelines on cardiovascular disease prevention in clinical practice. (2016, background): “appears to enhance CV risk directly and indirectly via accentuation of existing risk pathways.(178) While early small studies suggested RA increases CV risk beyond other risk markers, the recent analysis of”
Guidelines on cardiovascular disease prevention in clinical practice: the European perspective (2005, positive): “There is now clear evidence implicating high-grade inflammation as a pathway for 1153 accelerated vascular disease.(180) Systemic inflammation appears to enhance CV risk directly 1154 and indirectly via accentuation of existing risk pathways.”
Oxidation in rheumatoid arthritis (2004, neutral): “sclerosis in RA [54–56].”
IL-6 receptor inhibition with tocilizumab improves treatment outcomes in patients with rheumatoid arthritis refractory to anti-tumour necrosis factor biologicals: results from a 24-week multicentre randomised placebo-controlled trial (2008, background): “38 40–43 Interestingly, the ApoB/ApoA ratio is viewed as possibly the more relevant indicator for inflammatory vascular disorders than other atherogenic indices, and this index worsened in a comparable proportion ( , 10”
Cytokines in the pathogenesis of rheumatoid arthritis (2007, background): “Several pro-inflammatory cytokines probably drive the accelerated vascular disease that has been described in patients with rheumatoid arthritis and contribute directly to altered function of adipocytes (including adipocytokine release), lipid metabolism, insulin resistance and acquired metabolic sy”
Comparison of tocilizumab monotherapy versus methotrexate monotherapy in patients with moderate to severe rheumatoid arthritis: the AMBITION study (2009, background): “34 Although cardiovascular events were not seen in patients with these elevations during this study, treatment according to guidelines is recommended to deal with cardiovascular risk, and there remains a need for longer-term follow-up during chronic treatment to determine any implications of this…”
Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis (2006, positive): “patients with RA bearing an enhanced risk for insulin resistance and cardiovascular disease [24] led us to investigate these association in patients with psoriasis and PsA.”