Background: Atherosclerotic plaque is subjected to a repetitive deformation due to\r\narterial pulsatility during each cardiac cycle and damage may be accumulated over a\r\ntime period causing fibrous cap (FC) fatigue, which may ultimately lead to rupture. In\r\nthis study, we investigate the fatigue process in human carotid plaques using in vivo\r\ncarotid magnetic resonance (MR) imaging.\r\nMethod: Twenty seven patients with atherosclerotic carotid artery disease were\r\nincluded in this study. Multi-sequence, high-resolution MR imaging was performed\r\nto depict the plaque structure. Twenty patients were found with ruptured FC or\r\nulceration and 7 without. Modified Paris law was used to govern crack propagation\r\nand the propagation direction was perpendicular to the maximum principal stress at\r\nthe element node located at the vulnerable site.\r\nResults: The predicted crack initiations from 20 patients with FC defect all matched\r\nwith the locations of the in vivo observed FC defect. Crack length increased rapidly\r\nwith numerical steps. The natural logarithm of fatigue life decreased linearly with the\r\nlocal FC thickness (R2 = 0.67). Plaques (n=7) without FC defect had a longer fatigue\r\nlife compared with those with FC defect (p = 0.03).\r\nConclusion: Fatigue process seems to explain the development of cracks in FC,\r\nwhich ultimately lead to plaque rupture.
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