Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study

Joao Daniel T. Fontes, Jennifer F. Yamamoto, Martin G. Larson, Na Wang, Dhayana Dallmeier, Michiel Rienstra, Renate B. Schnabel, Ramachandran S. Vasan, John F. Keaney, Emelia J. Benjamin

Research output: Contribution to journalArticle

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Abstract

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 r2 = 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.

Original languageEnglish (US)
Pages (from-to)217-223
Number of pages7
JournalAtherosclerosis
Volume228
Issue number1
DOIs
StatePublished - May 2013
Externally publishedYes

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Biomarkers
Phospholipases
Lipoproteins
Tumor Necrosis Factor Receptors
C-Reactive Protein
Inflammation
Isoprostanes
Osteoprotegerin
P-Selectin
Chemokine CCL2
Hormone Replacement Therapy
Intercellular Adhesion Molecule-1
Hypercholesterolemia
Statistical Factor Analysis
Interleukin-6
Body Mass Index
Smoking
Lipids

Keywords

  • Biological markers
  • Inflammation
  • Longitudinal studies

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Fontes, J. D. T., Yamamoto, J. F., Larson, M. G., Wang, N., Dallmeier, D., Rienstra, M., ... Benjamin, E. J. (2013). Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study. Atherosclerosis, 228(1), 217-223. https://doi.org/10.1016/j.atherosclerosis.2013.01.019

Clinical correlates of change in inflammatory biomarkers : The Framingham Heart Study. / Fontes, Joao Daniel T.; 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: Contribution to journalArticle

Fontes, JDT, Yamamoto, JF, Larson, MG, Wang, N, Dallmeier, D, Rienstra, M, Schnabel, RB, Vasan, RS, Keaney, JF & Benjamin, EJ 2013, 'Clinical correlates of change in inflammatory biomarkers: The Framingham Heart Study', Atherosclerosis, vol. 228, no. 1, pp. 217-223. https://doi.org/10.1016/j.atherosclerosis.2013.01.019
Fontes, Joao Daniel T. ; Yamamoto, Jennifer F. ; Larson, Martin G. ; Wang, Na ; Dallmeier, Dhayana ; Rienstra, Michiel ; Schnabel, Renate B. ; Vasan, Ramachandran S. ; Keaney, John F. ; Benjamin, Emelia J. / Clinical correlates of change in inflammatory biomarkers : The Framingham Heart Study. In: Atherosclerosis. 2013 ; Vol. 228, No. 1. pp. 217-223.
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abstract = "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 r2 = 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.",
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AU - Fontes, Joao Daniel T.

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.

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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 r2 = 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 r2 = 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.

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