Endothelial Dysfunction and Low-Grade Inflammation Are Associated With Greater Arterial Stiffness Over a 6-Year Period

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2011-10, Vol.58 (4), p.588-595
• Main Authors: van Bussel, Bas C, Schouten, Fleur, Henry, Ronald M, Schalkwijk, Casper G, de Boer, Michiel R, Ferreira, Isabel, Smulders, Yvo M, Twisk, Jos W, Stehouwer, Coen D
• Format: Article
• Language: English
• Subjects: Adult; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Biomarkers - blood; Blood and lymphatic vessels; Blood Flow Velocity - physiology; Brachial Artery - diagnostic imaging; Brachial Artery - physiopathology; C-Reactive Protein - metabolism; Cardiology. Vascular system; Cardiovascular Diseases - epidemiology; Cardiovascular Diseases - etiology; Cardiovascular Diseases - physiopathology; Carotid Arteries - diagnostic imaging; Carotid Arteries - physiopathology; Cytokines - blood; E-Selectin - blood; Elasticity - physiology; Endothelium, Vascular - physiopathology; Experimental diseases; Female; Femoral Artery - diagnostic imaging; Femoral Artery - physiopathology; Follow-Up Studies; Humans; Inflammation - blood; Inflammation - physiopathology; Longitudinal Studies; Male; Medical sciences; Risk Factors; Serum Amyloid A Protein - metabolism; Thrombomodulin - blood; Ultrasonography; von Willebrand Factor - metabolism
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/HYPERTENSIONAHA.111.174557

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.