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Cap inflammation leads to higher plaque cap strain and lower cap stress: An MRI-PET/CT-based FSI modeling approach.

Accepted version
Peer-reviewed

Type

Article

Change log

Authors

Tang, D 
Yang, C 
Huang, S 
Mani, V 
Zheng, J 

Abstract

Plaque rupture may be triggered by extreme stress/strain conditions. Inflammation is also implicated and can be imaged using novel imaging techniques. The impact of cap inflammation on plaque stress/strain and flow shear stress were investigated. A patient-specific MRI-PET/CT-based modeling approach was used to develop 3D fluid-structure interaction models and investigate the impact of inflammation on plaque stress/strain conditions for better plaque assessment. 18FDG-PET/CT and MRI data were acquired from 4 male patients (average age: 66) to assess plaque characteristics and inflammation. Material stiffness for the fibrous cap was adjusted lower to reflect cap weakening causing by inflammation. Setting stiffness ratio (SR) to be 1.0 (fibrous tissue) for baseline, results for SR=0.5, 0.25, and 0.1 were obtained. Thin cap and hypertension were also considered. Combining results from the 4 patients, mean cap stress from 729 cap nodes was lowered by 25.2% as SR went from 1.0 to 0.1. Mean cap strain value for SR=0.1 was 0.313, 114% higher than that from SR=1.0 model. The thin cap SR=0.1 model had 40% mean cap stress decrease and 81% cap strain increase compared with SR=1.0 model. The hypertension SR=0.1 model had 19.5% cap stress decrease and 98.6% cap strain increase compared with SR=1.0 model. Differences of flow shear stress with 4 different SR values were limited (<10%). Cap inflammation may lead to large cap strain conditions when combined with thin cap and hypertension. Inflammation also led to lower cap stress. This shows the influence of inflammation on stress/strain calculations which are closely related to plaque assessment.

Description

Keywords

Arteriosclerosis, Inflammation, Plaque rupture, Stress, Vulnerable plaque

Journal Title

Journal of Biomechanics

Conference Name

Journal ISSN

0021-9290
1873-2380

Volume Title

50

Publisher

Elsevier BV
Sponsorship
This work was supported in part by NIH grants NIH/NIBIB R01 EB004759, NIH/NHLBI R01 HL071021, and National Natural Sciences Foundation of China grant 11672001, 11171030.