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Updated: Jun 17, 2026
A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Association of interleukin-18 levels with global arterial function and early structural changes in men without
Charalambos Vlachopoulos1, Nikolaos Ioakeimidis, Konstantinos Aznaouridis
1Peripheral Vessels Unit, 1st Cardiology Department, Athens Medical School, Hippokration Hospital, Athens, Greece. cvlachop@otenet.gr
Background:
Increased levels of interleukin-18 (IL-18) have been related to plaque progression and vulnerability and cardiovascular outcomes. Arterial functional and structural characteristics and endothelial/inflammatory activation are important determinants of cardiovascular performance and predictors of risk. We investigated whether IL-18 is a determinant of global arterial function and early structural changes in men.
Methods:
We evaluated arterial structural and functional characteristics (carotid-femoral pulse wave velocity (PWV), central aortic pressures, wave reflection indexes, flow-mediated dilation of the brachial artery, and common carotid intima-media thickness (IMT)) and we measured systemic inflammatory markers in 97 men (mean age 57.8 +/- 8.6 years) without manifest cardiovascular/atherosclerotic disease.
Results:
Multivariable analysis adjusting for age, mean pressure, other risk factors, high-sensitivity C-reactive protein (hsCRP), and treatment showed independent associations between IL-18 level and carotid-femoral PWV (P < 0.01) and IMT (P = 0.03). On the other hand, no relationship between IL-18 and flow-mediated dilation, central pressures or augmentation index (AIx) was found. The combination of higher IL-18 level with higher carotid-femoral PWV and carotid IMT values showed greater effect on 10-year risk of a cardiovascular event.
Conclusions:
IL-18 level is independently associated with aortic stiffening and carotid early atherosclerosis. This finding underlines the important role of IL-18 as a marker of arterial damage, and implies a contribution of this compound to the pathophysiology of cardiovascular disease.
