Advanced human carotid plaque progression correlates positively with flow shear stress using follow-up scan data: an in vivo MRI multi-patient 3D FSI study.
Advanced human carotid plaque progression correlates positively with flow shear stress using follow-up scan data: an in vivo MRI multi-patient 3D FSI study.
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DOI:
10.1016/j.jbiomech.2010.05.018
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发表时间:
2010-09-17
影响因子:
2.4
通讯作者:
Tang, Dalin
中科院分区:
文献类型:
--
作者:
Yang, Chun;Canton, Gador;Yuan, Chun;Ferguson, Marina;Hatsukami, Thomas S.;Tang, Dalin
Although it has been well-accepted that atherosclerosis initiation and early progression correlate negatively with flow wall shear stresses (FSS), increasing evidence suggests mechanisms governing advanced plaque progression are not well understood. Fourteen patients were scanned 2–4 times at 18 month intervals using a histologically validated multi-contrast magnetic resonance imaging (MRI) protocol to acquire carotid plaque progression data. Thirty-two scan pairs (baseline and follow-up scans) were formed with slices matched for model construction and analysis. 3D fluid-structure interaction (FSI) models were constructed and plaque wall stress (PWS) and flow shear stress (FSS) were obtained from all matching lumen data points (400–1000 per plaque; 100 points per matched slice) to quantify correlations with plaque progression measured by vessel wall thickness increase (WTI). Using FSS and PWS data from follow-up scan, 21 out of 32 scan pairs showed a significant positive correlation between WTI and FSS (positive/negative/no significance ratio = 21/8/3), and 26 out of 32 scan pairs showed a significant negative correlation between WTI and PWS (positive/negative/no significance ratio = 2/26/4). The mean FSS value of lipid core nodes (n=5294) from all 47 plaque models was 63.5 dyn/cm2, which was 45% higher than that from all normal vessel nodes (n=27553, p<0.00001)). The results from this intensive FSI study indicate that flow shear stress from follow-up scan correlates positively with advanced plaque progression which is different from what has been observed in plaque initiation and early-stage progression. It should be noted that the correlation results do not automatically lead to any causality conclusions.
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DOI:
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