Abstract
Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease. Arterial stiffening plays an important role in cardiovascular disease and, thus, may be a mechanism through which endothelial dysfunction and/or low-grade inflammation lead to cardiovascular disease. We investigated the associations between, on the one hand, biomarkers of endothelial dysfunction (soluble endothelial selectin, thrombomodulin, and both vascular and intercellular adhesion molecules 1 and von Willebrand factor) and of low-grade inflammation (C-reactive protein, serum amyloid A, interleukin 6, interleukin 8, tumor necrosis factor-α and, soluble intercellular adhesion molecule 1) and, on the other hand, arterial stiffness over a 6-year period, in 293 healthy adults (155 women). Biomarkers were combined into mean z scores. Carotid, femoral, and brachial arterial stiffness and carotid-femoral pulse wave velocity were determined by ultrasonography. Measurements were obtained when individuals were 36 and 42 years of age. Associations were analyzed with generalized estimating equation and adjusted for sex, height, and mean arterial pressure. The endothelial dysfunction z score was inversely associated with femoral distensibility (β: -0.51 [95% CI: -0.95 to -0.06]) and compliance coefficients (β: -0.041 [95% CI: -0.076 to -0.006]) but not with carotid or brachial stiffness or carotid-femoral pulse wave velocity. The low-grade inflammation z score was inversely associated with femoral distensibility (β: -0.51 [95% CI: -0.95 to -0.07]) and compliance coefficients (β: -0.050 [95% CI: -0.084 to -0.016]) and with carotid distensibility coefficient (β: -0.910 [95% CI: -1.810 to -0.008]) but not with brachial stiffness or carotid-femoral pulse wave velocity. Biomarkers of endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness. This provides evidence that arterial stiffening may be a mechanism through which endothelial dysfunction and low-grade inflammation lead to cardiovascular disease.
Highlights
Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease
In the analyses for the individual elements of the low-grade inflammation z score, the results showed that ln serum amyloid A and lnCRP were the strongest determinants of the carotid artery DC (Figure A), whereas sICAM-1 and ln interleukin 6 were the strongest determinants of the femoral artery DC (Figure B) and sICAM-1 and lnCRP were the strongest determinants for the femoral artery CC (Figure C)
Biomarker scores for endothelial dysfunction and low-grade inflammation were associated with greater arterial stiffness over a 6-year period
Summary
Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease. The endothelial dysfunction z score was inversely associated with femoral distensibility (: Ϫ0.51 [95% CI: Ϫ0.95 to Ϫ0.06]) and compliance coefficients (: Ϫ0.041 [95% CI: Ϫ0.076 to Ϫ0.006]) but not with carotid or brachial stiffness or carotid-femoral pulse wave velocity. Biomarkers of endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness This provides evidence that arterial stiffening may be a mechanism through which endothelial dysfunction and low-grade inflammation lead to cardiovascular disease. From observational studies,[1,2,3,4,5] it has become increasingly clear that biomarkers of endothelial dysfunction and low-grade inflammation are closely associated with (incident) cardiovascular disease In part, these associations can be explained by the fact that endothelial dysfunction and lowgrade inflammation play key roles in atherothrombosis.[6] other mechanisms may be important. We have investigated the 6-year longitudinal associations between biomarkers of endothelial dysfunction and low-grade inflammation, on the one hand, and stiffness estimates of the carotid, femoral, and brachial arteries and of the carotid-femoral segment, on the other, in apparently healthy adults of the Amsterdam Growth and Health Longitudinal Study
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