Abstract
Growth, ageing and atherosclerotic plaque development alter the biomechanical forces acting on the vessel wall. However, monitoring the detailed local changes in wall shear stress (WSS) at distinct sites of the murine aortic arch over time has been challenging. Here, we studied the temporal and spatial changes in flow, WSS, oscillatory shear index (OSI) and elastic properties of healthy wildtype (WT, n = 5) and atherosclerotic apolipoprotein E-deficient (Apoe−/−, n = 6) mice during ageing and atherosclerosis using high-resolution 4D flow magnetic resonance imaging (MRI). Spatially resolved 2D projection maps of WSS and OSI of the complete aortic arch were generated, allowing the pixel-wise statistical analysis of inter- and intragroup hemodynamic changes over time and local correlations between WSS, pulse wave velocity (PWV), plaque and vessel wall characteristics. The study revealed converse differences of local hemodynamic profiles in healthy WT and atherosclerotic Apoe−/− mice, and we identified the circumferential WSS as potential marker of plaque size and composition in advanced atherosclerosis and the radial strain as a potential marker for vascular elasticity. Two-dimensional (2D) projection maps of WSS and OSI, including statistical analysis provide a powerful tool to monitor local aortic hemodynamics during ageing and atherosclerosis. The correlation of spatially resolved hemodynamics and plaque characteristics could significantly improve our understanding of the impact of hemodynamics on atherosclerosis, which may be key to understand plaque progression towards vulnerability.
Highlights
This article is an open access articleAtherosclerosis is a complex inflammatory disease, characterized by the formation of fibrofatty lesions in the intimal layer of the artery wall [1].Ruptures or erosions of these plaques are responsible for most of the cardiovascular events in the Western world, including myocardial infarction and stroke
While the weight of WT mice increased over time, no significant changes were observed in Apolipoprotein E-deficient (Apoe)−/− mice, with no significant differences between the groups (Supplementary Figure S1A)
Both mouse groups showed an increase in aortic volumes over time; 24week-old Apoe−/− mice featured significantly smaller mean volumes compared with the control group (Figure 3A)
Summary
This article is an open access articleAtherosclerosis is a complex inflammatory disease, characterized by the formation of fibrofatty lesions in the intimal layer of the artery wall (atherosclerotic plaques) [1].Ruptures or erosions of these plaques are responsible for most of the cardiovascular events in the Western world, including myocardial infarction and stroke. Atherosclerosis is a complex inflammatory disease, characterized by the formation of fibrofatty lesions in the intimal layer of the artery wall (atherosclerotic plaques) [1]. Biomedicines 2021, 9, 1856 cause an endothelial dysfunction in the whole arterial tree, plaques develop mainly at predilection sites, such as curvatures, branch points and bifurcations [2,3]. These regions are characterized by low and oscillatory wall shear stress (WSS) that cause an endothelial dysfunction, which, together with other processes, such as lipid deposition, determine the location of plaque development [4,5]. The growing plaque leads to structural and mechanical changes in the vessel wall due to vascular remodeling and narrowing, enhancing disturbed flow patterns and affecting local WSS
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