Study of carotid arterial plaque stress for symptomatic and asymptomatic patients

Abstract

Stroke is one of the leading causes of death in the world, resulting mostly from the sudden ruptures of atherosclerosis carotid plaques. Until now, the exact plaque rupture mechanism has not been fully understood, and also the plaque rupture risk stratification. The advanced multi-spectral magnetic resonance imaging (MRI) has allowed the plaque components to be visualized in-vivo and reconstructed by computational modeling. In the study, plaque stress analysis using fully coupled fluid structure interaction was applied to 20 patients (12 symptomatic and 8 asymptomatic) reconstructed from in-vivo MRI, followed by a detailed biomechanics analysis, and morphological feature study. The locally extreme stress conditions can be found in the fibrous cap region, 85% at the plaque shoulder based on the present study cases. Local maximum stress values predicted in the plaque region were found to be significantly higher in symptomatic patients than that in asymptomatic patients (200±43 kPa vs. 127±37 kPa, p=0.001). Plaque stress level, defined by excluding 5% highest stress nodes in the fibrous cap region based on the accumulative histogram of stress experienced on the computational nodes in the fibrous cap, was also significantly higher in symptomatic patients than that in asymptomatic patients (154±32 kPa vs. 111±23 kPa, p<0.05). Although there was no significant difference in lipid core size between the two patient groups, symptomatic group normally had a larger lipid core and a significantly thinner fibrous cap based on the reconstructed plaques using 3D interpolation from stacks of 2D contours. Plaques with a higher stenosis were more likely to have extreme stress conditions upstream of plaque throat. The combined analyses of plaque MR image and plaque stress will advance our understanding of plaque rupture, and provide a useful tool on assessing plaque rupture risk.

Introduction

Atherosclerosis is one of the leading causes of death all over the world, caused by plaque rupture and subsequent thrombus formation (Rosamond et al., 2007). Despite many years of research, the underlying mechanism for plaque rupture is still not fully understood (Naghavi et al., 2003). It is believed that several factors play important roles in the rupture process: (a) biological abnormalities, such as enhanced inflammatory activity, and the accumulation of macrophages (Libby et al., 2002); (b) biomechanical factors, such as local extreme mechanical stress (Cheng et al., 1993, Lee et al., 1993, Ohayon et al., 2001, Richardson et al., 1989). With recent development of imaging techniques and the improved understanding of plaque rupture mechanisms, it is increasingly becoming clear that plaque vulnerability cannot be described by the degree of stenosis alone (Giroud et al., 1992). It has been suggested that plaque morphology, plaque biomechanical environment, and inflammation activity will all influence their vulnerability (Richardson, 2002, Naghavi and Libby, 2003, Ohayon et al., 2008). From biomechanical aspect, the rupture can be considered to be a mechanical failure event. Therefore it is useful to study the detailed mechanical stress distribution on specific plaques in order to develop a more precise assessment of the risk of plaque rupture (Zheng et al., 2005, Li et al., 2006).

Patient specific plaque stress analysis has been providing critical information on the understanding of plaque rupture mechanisms and may eventually lead to rupture risk assessment (Tang et al., 2005a). Recent developments in high-resolution multi-spectral MRI have allowed plaque components to be visualized in-vivo (Hatsukami et al., 2000, Cai et al., 2002, Yuan et al., 2002), providing more realistic plaque geometries for stress analysis (Touze et al., 2007, Gao et al., 2009a). Based on 2D in-vivo MRI, Li et al. (2007) found that stress in asymptomatic patients was lower than that in symptomatic patients. Stress analysis by fluid structure interaction (FSI) has gained popularity for providing more realistic results recently (Tang et al., 2004). Gao et al. (2009b) studied carotid plaque stress distribution using FSI based on in-vivo MR images from 4 patients, and a risk assessment was made from the analysis. Based on 12 carotid plaques, Tang et al. (2009) compared plaque stress between a group of 5 ruptured plaques and 7 un-ruptured plaques using FSI methods. They found that stress in the rupture sites was significantly higher than in the surrounding region; the mean critical principal wall stress was significantly higher in the ruptured group than in the non-ruptured group, which may provide important evidence for plaque rupture induced by high mechanical stress.

In this study, we report our latest result of plaque stress analysis on a larger group of 20 patients in which 12 were symptomatic and 8 were asymptomatic. The 20 carotid plaque models were reconstructed from in-vivo MR images. The fully coupled FSI simulation was performed on each patient, and followed by a detailed stress analysis. Plaque wall stress and related morphological features were compared between the symptomatic and asymptomatic patients.