Studying the Factors of Human Carotid Atherosclerotic Plaque Rupture, by Calculating Stress/Strain in the Plaque, Based on CEUS Images: A Numerical Study

Abstract

Carotid plaque neovascularization is one of the major factors for the classification of vulnerable plaque, but the axial force effects of the pulsatile blood flow on the plaque with neovessel and intraplaque hemorrhage was unclear. Together with the severity of stenosis, the fibrous cap thickness, large lipid core, and the neovascularization followed by intraplaque hemorrhage (IPH) have been regarded as high-risk features of plaque rupture. In this work, the effects of these factors were evaluated on the progression and rupture of the carotid atherosclerotic plaques. Five geometries of carotid artery plaque were developed based on contrast-enhanced ultrasound (CEUS) images, which contain two types of neovessel and IPH, and geometry without neovessel and IPH. A one-way fluid-structure interaction model was applied to compute the maximum principal stress and strain in the plaque. For that hyper-elastic and non-linear material, Yeoh 3rd Order strain energy density function was used for components of the plaque. The simulation results indicated that the maximum principal stress of plaque in the carotid artery was higher when the degree of the luminal stenosis increased and the thickness of the fibrous cap decreased. The neovessels within the plaque could introduce a 2.5% increments of deformation in the plaque under the pulsatile blood flow pressure. The IPH also contributed to the increased risk of plaque rupture that a gain of stress was 8.983, 14.526, and 34.47 kPa for the plaque with 50, 65, and 75%, respectively, when comparing stress in the plaque with IPH distributed at the middle to the shoulder of the plaque. In conclusion, neovascularization in the plaque could reduce the stability of the plaque by increasing the stress within the plaque. Also, the risk of plaque rupture increased when large luminal stenosis, thin fibrous cap, and IPH were observed.

Noninvasive assessment of carotid plaque with subharmonic aided pressure estimation from a US contrast agent: A preliminary study

“…Related studies have illustrated that neovascularization and hemorrhage in plaque increase the pressure in plaque. 33 This also confirmed the conclusion of previous research of which the limitation of carotid stenosis in evaluating the occurrence of stroke and the importance of assessing the internal composition and morphological changes of large artery stroke. 37,38 In the current study, we observed that the subharmonic gradient of intraplaque was relatively larger in the IS group, and the threshold value of 3.95 dB was obtained, with specificity of about 77.27% and sensitivity of about 66.67%, which provides a new way for us to quantitatively monitor the pressure in plaque.…”

“…Therefore, the high‐pressure difference on the plaque surface may induce the plaque to break easily. Related studies have illustrated that neovascularization and hemorrhage in plaque increase the pressure in plaque 33 . This also confirmed the conclusion of previous research of which the limitation of carotid stenosis in evaluating the occurrence of stroke and the importance of assessing the internal composition and morphological changes of large artery stroke 37,38 .…”

“…When the plaque became thicker, the relative surface area of the plaque expanded, the fibrous cap on the surface of the plaque got uneven and thinner, the grade of neovascularization and lumen stenosis degree increased 32 . Consequently, the stress of the plaque increased significantly 33 …”

“…32 Consequently, the stress of the plaque increased significantly. 33 Therefore, in further analysis, we found that IMT in the IS group was thicker than that in the control group as in previous studies, 34 and our results also indicate that, through the quantitative analysis of SHAPE US, the subharmonic gradient intra the plaque of the IS group was higher than that in the control group with the quantitative analysis of SHAPE US, but there was no difference between the groups in the stenosis rate, the subharmonic gradient across the cap, etc. From the perspective of hemodynamic, after the formation of plaque, the blood flow through the lumen was unchanged in unit time.…”

Emerging Role of Carotid MRI for Personalized Ischemic Stroke Risk Prediction in Patients With Carotid Artery Stenosis

“…Apoptosis and necrosis of the foam cells leads to the build-up of a lipid-rich necrotic core (LRNC). Plaque neovessels support the entry of more monocytes into the plaque, however, these vessels are fragile, which could cause intraplaque hemorrhage (IPH) ( 14 ). Also fissures or disruption of the fibrous cap (FC) may contribute to the development of IPH ( 15 ).…”