Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study
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Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study. / Fontes, Joao D; Yamamoto, Jennifer F; Larson, Martin G; Wang, Na; Dallmeier, Dhayana; Rienstra, Michiel; Schnabel, Renate B; Vasan, Ramachandran S; Keaney, John F; Benjamin, Emelia J.
In: ATHEROSCLEROSIS, Vol. 228, No. 1, 05.2013, p. 217-223.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study
AU - Fontes, Joao D
AU - Yamamoto, Jennifer F
AU - Larson, Martin G
AU - Wang, Na
AU - Dallmeier, Dhayana
AU - Rienstra, Michiel
AU - Schnabel, Renate B
AU - Vasan, Ramachandran S
AU - Keaney, John F
AU - Benjamin, Emelia J
N1 - Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
PY - 2013/5
Y1 - 2013/5
N2 - OBJECTIVES: Traditional clinical risk factors are associated with inflammation cross-sectionally, but associations of longitudinal variation in inflammatory biomarkers with corresponding changes in clinical risk factors are incompletely described. We sought to analyze clinical factors associated with change in inflammation in the community.METHODS: We studied 3013 Framingham Offspring (n = 2735) and Omni Cohort (n = 278) participants (mean age 59 years, 55% women, 9% ethnic/racial minority) who attended two consecutive examination cycles (mean 6.7 years apart). We selected ten inflammatory biomarkers representing distinctive biological functions: C-reactive protein (CRP), intercellular adhesion molecule-1, interleukin-6, isoprostanes, lipoprotein-associated phospholipase-2 (Lp-PLA2) activity, Lp-PLA2-mass, monocyte chemoattractant protein-1, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II (TNFRII). We constructed multivariable-adjusted regression models to assess the relations of baseline, follow-up and change in clinical risk factors with change in biomarker concentrations over time.RESULTS: Baseline, follow-up and change in clinical risk factors explain a moderate amount of the variation in biomarker concentrations across 2 consecutive examinations (ranging from r(2) = 0.28 [TNFRII] up to 0.52 [Lp-PLA2-mass]). In multivariable models, increasing body-mass index, smoking initiation, worsening lipid profile, and increasing waist size were associated with increasing concentrations of several biomarkers. Conversely, hypercholesterolemia therapy and hormone replacement cessation were associated with decreasing concentrations of biomarkers such as CRP, Lp-PLA2-mass and activity.CONCLUSION: Cardiovascular risk factors have different patterns of association with longitudinal change in inflammatory biomarkers and explain modest amounts of variability in biomarker concentrations. Nevertheless, a substantial proportion of longitudinal change in inflammatory markers is not explained by traditional risk factors.
AB - OBJECTIVES: Traditional clinical risk factors are associated with inflammation cross-sectionally, but associations of longitudinal variation in inflammatory biomarkers with corresponding changes in clinical risk factors are incompletely described. We sought to analyze clinical factors associated with change in inflammation in the community.METHODS: We studied 3013 Framingham Offspring (n = 2735) and Omni Cohort (n = 278) participants (mean age 59 years, 55% women, 9% ethnic/racial minority) who attended two consecutive examination cycles (mean 6.7 years apart). We selected ten inflammatory biomarkers representing distinctive biological functions: C-reactive protein (CRP), intercellular adhesion molecule-1, interleukin-6, isoprostanes, lipoprotein-associated phospholipase-2 (Lp-PLA2) activity, Lp-PLA2-mass, monocyte chemoattractant protein-1, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II (TNFRII). We constructed multivariable-adjusted regression models to assess the relations of baseline, follow-up and change in clinical risk factors with change in biomarker concentrations over time.RESULTS: Baseline, follow-up and change in clinical risk factors explain a moderate amount of the variation in biomarker concentrations across 2 consecutive examinations (ranging from r(2) = 0.28 [TNFRII] up to 0.52 [Lp-PLA2-mass]). In multivariable models, increasing body-mass index, smoking initiation, worsening lipid profile, and increasing waist size were associated with increasing concentrations of several biomarkers. Conversely, hypercholesterolemia therapy and hormone replacement cessation were associated with decreasing concentrations of biomarkers such as CRP, Lp-PLA2-mass and activity.CONCLUSION: Cardiovascular risk factors have different patterns of association with longitudinal change in inflammatory biomarkers and explain modest amounts of variability in biomarker concentrations. Nevertheless, a substantial proportion of longitudinal change in inflammatory markers is not explained by traditional risk factors.
KW - 1-Alkyl-2-acetylglycerophosphocholine Esterase/blood
KW - Aged
KW - Biomarkers/blood
KW - C-Reactive Protein/metabolism
KW - Cardiovascular Diseases/epidemiology
KW - Chemokine CCL2/blood
KW - Female
KW - Humans
KW - Inflammation/epidemiology
KW - Intercellular Adhesion Molecule-1/blood
KW - Interleukin-6/blood
KW - Isoprostanes/blood
KW - Longitudinal Studies
KW - Male
KW - Massachusetts/epidemiology
KW - Middle Aged
KW - Osteoprotegerin/blood
KW - P-Selectin/blood
KW - Receptors, Tumor Necrosis Factor, Type II/blood
KW - Risk Factors
KW - Vasculitis/epidemiology
U2 - 10.1016/j.atherosclerosis.2013.01.019
DO - 10.1016/j.atherosclerosis.2013.01.019
M3 - SCORING: Journal article
C2 - 23489346
VL - 228
SP - 217
EP - 223
JO - ATHEROSCLEROSIS
JF - ATHEROSCLEROSIS
SN - 0021-9150
IS - 1
ER -
