Impact of Fiber Structure on the Material Stability and Rupture Mechanisms of Coronary Atherosclerotic Plaques

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Douglas, G 
Brown, A 

The rupture of an atherosclerotic plaque in the coronary circulation remains the main cause of heart attack. As a fiber-oriented structure, the fiber structure, in particular in the fibrous cap (FC), may affect both loading and material strength in the plaque. However, the role of fiber orientation and dispersion in plaque rupture is unclear. Local orientation and dispersion of fibers were calculated for the shoulder regions, mid FC, and regions with intimal thickening (IT) from histological images of 16 human coronary atherosclerotic lesions. Finite element analysis was performed to assess the effect of these properties on mechanical conditions. Fibers in shoulder regions had markedly reduced alignment (Median [interquartile range] 12.9° [6.6, 18.0], p <0.05) compared with those in mid FC (6.1° [5.5, 9.0]) and IT regions (6.7° [5.1, 8.6]). Fiber dispersion was highest in shoulders (0.150 [0.121, 0.192]), intermediate in IT (0.119 [0.103, 0.144]), and lowest in mid FC regions (0.093 [0.081, 0.105], p <0.05). When anisotropic properties were considered, stresses were significantly higher for the mid FC (p = 0.030) and IT regions (p = 0.002) and no difference was found for the shoulder or global regions. Shear (sliding) stress between fibers in each region and their proportion of maximum principal stress were: shoulder (25.8 kPa [17.1, 41.2], 12.4%), mid FC (13.9 kPa [5.8, 29.6], 13.8%), and IT (36.5 kPa [25.9, 47.3], 15.5%). Fiber structure within the FC has a marked effect on principal stresses, resulting in considerable shear stress between fibers. Fiber structure including orientation and dispersion may determine mechanical strength and thus rupture of atherosclerotic plaques. K

coronary, atherosclerosis, rupture, fiber, stress
Journal Title
Annals of Biomedical Engineering
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Heart Research UK (RG2638/14/16)
Medical Research Council (MC_PC_15042)
This research is supported by HRUK (RG2638/14/ 16), NSERC (6799-427538-2012), the WD Armstrong Trust, and the NIHR Cambridge Biomedical Research Centre.