Abstract
We examined the potential impact of conventional compared with nonconventional cardiovascular risk factors including interleukin-6 levels on endothelial activation in RA. Circulating soluble E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and monocyte chemoattractant protein-1 concentrations were measured in 217 African patients (112 black and 105 white) with RA. In comprehensive confounder adjusted mixed regression models, 5 conventional and 4 nonconventional cardiovascular risk factors were associated (P = 0.05 to <0.0001) with endothelial activation. Interleukin-6 was the only risk factor related to each endothelial activation molecule and independently contributed by 18% and significantly more than other risk factors to the variation in overall endothelial activation as estimated by an SD (z) score of endothelial activation molecule concentrations. The independent interleukin-6-overall endothelial activation relationships were reproduced in various subgroups. Interleukin-6 concentrations relate consistently, markedly, and to a larger extent than other cardiovascular risk factors to endothelial activation in RA. Assessment of interleukin-6 concentrations may enhance cardiovascular risk stratification in RA.
Highlights
Atherogenesis is increasingly recognized as a dynamic and inflammatory process [1,2,3] and is initiated by activation of endothelial cells upon exposure to cardiovascular risk factors. This results in enhanced expression of soluble forms of selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1)
We systematically examined the potential impact of conventional compared with non-conventional cardiovascular risk factors including IL-6 on endothelial activation in a relatively large RA cohort
Population grouping impacted on the relationship between IL-6 and monocyte chemoattractant protein-1 (MCP-1) concentrations
Summary
Atherogenesis is increasingly recognized as a dynamic and inflammatory process [1,2,3] and is initiated by activation of endothelial cells upon exposure to cardiovascular risk factors. This results in enhanced expression of soluble forms of selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1). Monocytes penetrate the endothelial lining and enter the intima of the arterial wall by diapedesis between endothelial cells. This monocyte transmigration is largely effectuated by monocyte chemoattractant protein-1 (MCP-1). MCP-1 plays a unique and crucial role in the initiation of atherosclerosis [4]
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