Circulation. 2003;108:2957-2963
doi: 10.1161/01.CIR.0000099844.31524.05
doi: 10.1161/01.CIR.0000099844.31524.05
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(Circulation. 2003;108:2957.)
© 2003 American Heart Association, Inc.
Review: Current Perspective |
Explaining How "High-Grade" Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis
From the Department of Pathological Biochemistry and Centre for Rheumatic Diseases, North Glasgow Hospitals University NHS Trust, Glasgow Royal Infirmary, Glasgow, Scotland.
Correspondence to Dr Naveed Sattar, Department of Pathological Biochemistry, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, UK. E-mail nsattar{at}clinmed.gla.ac.uk
There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Early epidemiological observational and clinical studies are commensurate with this hypothesis. By contrast, risk factor modulation with conventional agents, such as statins, may provide unpredictable clinical benefit in the context of uncontrolled systemic inflammatory parameters. Unraveling such complex relationships in which exaggerated inflammation–risk factor interactions are prevalent may elicit novel insights to effector mechanisms in vascular disease generally.
Key Words: immune system • risk factors • atherosclerosis
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