Viscoelastic properties of normal and atherosclerotic carotid arteries

Background: remodelling of the arterial wall occurs with ageing, even in the absence of atherosclerotic risk factors. With increasing age, arteries dilate, thicken, and get stiffer. The aim of this study was to correlate carotid artery stiffness with wall thickness and plaque presence between healthy individuals and patients with early and advanced atherosclerosis. Methods: twenty healthy volunteers, 40 carotid segments and 90 patients, 174 carotid segments, with vascular disease were included in the study. The carotid artery was imaged longitudinally and measurements of the intimal-medial thickness (IMT) and plaque were obtained. Systolic and diastolic blood pressures were taken from each arm. The carotid artery stiffness (pressure-strain elastic modulus, E-p) was calculated in all sites from the changes in pressure and diameter. M-mode was used to detect the diameter change (systolic to diastolic) over five cardiac cycles. Results: in the healthy volunteers there was no evidence of plaque or increased IMT. The mean IMT was significantly higher in the patients compared to control (0.83 +/- 0.27 mm vs. 0.54 +/- 0.08 mm, p < 0.0001). The IMT had a poor correlation with E-p at lower thickness (r = 0.24, p = 0.08) but this association became stronger with increasing thickness (r = 0.62, p < 0.001). Arterial segments with an IMT greater than or equal to 0.88 mm became significantly stiffer compared to the controls (p < 0.001) and to patients with an IMT < 0.88 mm (p < 0.01). Carotid E-p was markedly greater in arterial segments with plaques than in those with increased IMT (p < 0.001) and the controls (p < 0.0001). Conclusions: carotid wall areas with small increase in IMT have a poor correlation with carotid artery stiffness. The carotid stiffness increases in areas with marked wall thickening and particularly in segments with plaque. The simultaneous study of vessel-wall elastic behaviour with IMT and plaque changes may increase our understanding of atherosclerotic progression and wall remodelling.