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In vivo MRI-based simulation of fatigue process: a possible trigger for human carotid atherosclerotic plaque rupture
Yuan Huang1  Zhongzhao Teng3  Umar Sadat2  Jing He1  Martin J Graves1  Jonathan H Gillard1 
[1] University Department of Radiology, University of Cambridge, Level 5, Box 218, Hills Road, Addenbrooke’s Hospital, Cambridge, CB2 0QQ, UK
[2] Cambridge Vascular Unit, Addenbrooke’s Hospital, Cambridge, UK
[3] Department of Engineering, University of Cambridge, Cambridge, UK
关键词: Rupture;    Fatigue;    MRI;    Carotid;    Atherosclerosis;   
Others  :  797896
DOI  :  10.1186/1475-925X-12-36
 received in 2013-02-10, accepted in 2013-04-15,  发布年份 2013
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【 摘 要 】

Background

Atherosclerotic plaque is subjected to a repetitive deformation due to arterial pulsatility during each cardiac cycle and damage may be accumulated over a time period causing fibrous cap (FC) fatigue, which may ultimately lead to rupture. In this study, we investigate the fatigue process in human carotid plaques using in vivo carotid magnetic resonance (MR) imaging.

Method

Twenty seven patients with atherosclerotic carotid artery disease were included in this study. Multi-sequence, high-resolution MR imaging was performed to depict the plaque structure. Twenty patients were found with ruptured FC or ulceration and 7 without. Modified Paris law was used to govern crack propagation and the propagation direction was perpendicular to the maximum principal stress at the element node located at the vulnerable site.

Results

The predicted crack initiations from 20 patients with FC defect all matched with the locations of the in vivo observed FC defect. Crack length increased rapidly with numerical steps. The natural logarithm of fatigue life decreased linearly with the local FC thickness (R2 = 0.67). Plaques (n=7) without FC defect had a longer fatigue life compared with those with FC defect (p = 0.03).

Conclusion

Fatigue process seems to explain the development of cracks in FC, which ultimately lead to plaque rupture.

【 授权许可】

   
2013 Huang et al.; licensee BioMed Central Ltd.

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