Study of carotid arterial plaque stress for symptomatic and asymptomatic patients

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.     

Carotid arterial plaque stress analysis using fluid–structure interactive simulation based on in-vivo magnetic resonance images of four patients

The rupture of atherosclerotic plaques is known to be associated with the stresses that act on or within the arterial wall. The extreme wall tensile stress (WTS) is usually recognized as a primary trigger for the rupture of vulnerable plaque. The present study used the in-vivo high-resolution multi-spectral magnetic resonance imaging (MRI) for carotid arterial plaque morphology reconstruction. Image segmentation of different plaque components was based on the multi-spectral MRI and co-registered with different sequences for the patient. Stress analysis was performed on totally four subjects with different plaque burden by fluid–structure interaction (FSI) simulations. Wall shear stress distributions are highly related to the degree of stenosis, while the level of its magnitude is much lower than the WTS in the fibrous cap. WTS is higher in the luminal wall and lower at the outer wall, with the lowest stress at the lipid region. Local stress concentrations are well confined in the thinner fibrous cap region, and usually locating in the plaque shoulder; the introduction of relative stress variation during a cycle in the fibrous cap can be a potential indicator for plaque fatigue process in the thin fibrous cap. According to stress analysis of the four subjects, a risk assessment in terms of mechanical factors could be made, which may be helpful in clinical practice. However, more subjects with patient specific analysis are desirable for plaque-stability study.     

Mechanical stresses in carotid plaques using MRI-based fluid-structure interaction models

Risk assessment in patients with carotid atherosclerosis relies on the degree of luminal stenosis. Incorporating morphological information on plaque composition obtained noninvasively through the use of magnetic resonance imaging (MRI) could include other variables besides the degree of stenosis into carotid plaque risk assessment. Knowledge of the morphologic composition of the plaque allows determination of mechanic stresses exerted on the protective fibrous cap, which may be of importance in the assessment of plaque vulnerability. Based on image processing of transverse MRI scans, longitudinal 2D fluid-structure interaction (FSI) simulations of carotid atherosclerotic plaques were performed facilitating in-vivo estimation of longitudinal internal fibrous cap stresses. The FSI simulation combined finite element analysis (FEA) with computational fluid dynamics (CFD) simulations of blood-flow variables. Preliminary results from two symptomatic patients revealed longitudinal stress levels (max. 254.1 and 143.2 kPa) approaching established criteria for plaque rupture at known predilection sites of plaque rupture. Determination of longitudinal fibrous cap stresses may prove useful in assessing plaque vulnerability and improve risk stratification in patients with carotid atherosclerosis.     

Effects of varied lipid core volume and fibrous cap thickness on stress distribution in carotid arterial plaques

The rupture of atherosclerotic plaques is known to be associated with the stresses that act on or within the arterial wall. The extreme wall tensile stress is usually recognized as a primary trigger for the rupture of the plaque. The present study used one-way fluid-structure interaction simulation to investigate the impacts of fibrous cap thickness and lipid core volume to the wall tensile stress value and distributions on the fibrous cap. Von Mises stress was employed to represent the wall tensile stress (VWTS). A total of 13 carotid bifurcation cases were manipulated based on a base geometry in the study with varied combinations of fibrous cap thickness and lipid core volume in the plaque. Values of maximum VWTS and a stress value of VWTS_90, which represents the cut-off VWTS value of 90% in cumulative histogram of VWTS possessed at the computational nodes on the luminal surface of fibrous cap, were used to assess the risk of plaque rupture for each case. Both parameters are capable of separating the simulation cases into vulnerable and more stable plaque groups, while VWTS_90 is more robust for plaque rupture risk assessment. The results show that the stress level on the fibrous cap is much more sensitive to the changes in the fibrous cap thickness than the lipid core volume. A slight decrease of cap thickness can cause a significant increase of stress. For all simulation cases, high VWTS appears at the fibrous cap near the lipid core (plaque shoulder) regions.     

Fatigue and plaque rupture in myocardial infarction

Plaque rupture plays a role in the majority of acute coronary syndromes. Rupture has been associated with stress concentrations, which are affected by tissue properties and anatomy. In this study rupture was not approached as an acute syndrome, but rather as the culmination of a chronic injury or fatigue process. The aim of our study was to investigate the impact of anatomy, tissue properties, and blood pressure on a fatigue mechanism. Incremental crack propagation was dynamically simulated based on evolving stress distributions. Stresses were resolved by a finite element solver, using vessel stiffness properties derived from in vivo data. Plaque fatigue crack growth per pressure pulse was estimated using an adapted Paris-relation. It was demonstrated that cracks begin at the lumen wall at areas of stress concentration, depending on the shape of the lumen, thickness of the fibrous cap and stiffness of the plaque components. Mean or pulse pressure did not affect initiation location. Cracks extended radially and grew at a rate that was highly dependent on both mean and pulse pressure and on lipid stiffness. Rupture rate depended on blood pressure and lipid stiffness. It was concluded that a fatigue mechanism in a pulsatile cardiovascular pressure environment reconciles clinical evidence of acute plaque rupture at seemingly low stress levels, and it could provide a framework for developing strategies to create a biomechanically benign environment which is least conducive to plaque rupture.     

3D computational parametric analysis of eccentric atheroma plaque: influence of axial and circumferential residual stresses

Plaque rupture plays a role in the majority of acute coronary syndromes. Rupture has usually been associated with stress concentrations, which are mainly affected by the plaque geometry and the tissue properties. The aim of this study is to evaluate the influence of morphology on the risk of plaque rupture, including the main geometrical factors, and to assess the role of circumferential and axial residual stresses by means of a parametric 3D finite element model. For this purpose, a 3D parametric finite element model of the coronary artery with eccentric atheroma plaque was developed. Healthy (adventitia and media in areas without atheroma plaque) and diseased (fibrotic and lipidic) tissues were considered in the model. The geometrical parameters used to define and design the idealized coronary plaque anatomy were the lipid core length, the stenosis ratio, the fibrous cap thickness, and the lipid core ratio. Finally, residual stresses in longitudinal and circumferential directions were incorporated into the model to analyse the influence of the important mechanical factors in the vulnerability of the plaque. Viewing the results, we conclude that residual stresses should be considered in the modelling of this kind of problems since they cause a significant alteration of the vulnerable plaque region limits. The obtained results show that the fibrous cap thickness and the lipid core length, in combination with the lipid core width, appear to be the key morphological parameters that play a determinant role in the maximal principal stress (MPS). However, the stenosis ratio is found to not play a significant role in vulnerability related to the MPS. Plaque rupture should therefore be observed as a consequence, not only of the cap thickness, but as a combination of the stenosis ratio, the fibrous cap thickness and the lipid core dimensions.     

Mapping elasticity moduli of atherosclerotic plaque in situ via atomic force microscopy

Several studies have suggested that evolving mechanical stresses and strains drive atherosclerotic plaque development and vulnerability. Especially, stress distribution in the plaque fibrous capsule is an important determinant for the risk of vulnerable plaque rupture. Knowledge of the stiffness of atherosclerotic plaque components is therefore of critical importance. In this work, force mapping experiments using atomic force microscopy (AFM) were conducted in apolipoprotein E-deficient (ApoE(-/-)) mouse, which represents the most widely used experimental model for studying mechanisms underlying the development of atherosclerotic lesions. To obtain the elastic material properties of fibrous caps and lipidic cores of atherosclerotic plaques, serial cross-sections of aortic arch lesions were probed at different sites. Atherosclerotic plaque sub-structures were subdivided into cellular fibrotic, hypocellular fibrotic and lipidic rich areas according to histological staining. Hertz's contact mechanics were used to determine elasticity (Young's) moduli that were related to the underlying histological plaque structure. Cellular fibrotic regions exhibit a mean Young modulus of 10.4±5.7kPa. Hypocellular fibrous caps were almost six-times stiffer, with average modulus value of 59.4±47.4kPa, locally rising up to ～250kPa. Lipid rich areas exhibit a rather large range of Young's moduli, with average value of 5.5±3.5kPa. Such precise quantification of plaque stiffness heterogeneity will allow investigators to have prospectively a better monitoring of atherosclerotic disease evolution, including arterial wall remodeling and plaque rupture, in response to mechanical constraints imposed by vascular shear stress and blood pressure.     

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

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.     

The influence of vascular anatomy on carotid artery stenting: A parametric study for damage assessment

Carotid artery stenting is emerging as an alternative technique to surgery for the treatment of symptomatic severe carotid stenosis. Clinical and experimental evidence demonstrates that both plaque morphology and biomechanical changes due to the device implantation can be possible causes of an unsuccessful treatment. In order to gain further insights of the endovascular intervention, a virtual environment based on structural finite element simulations was built to emulate the stenting procedure on generalized atherosclerotic carotid geometries which included a damage model to quantify the injury of the vessel. Five possible lesion scenarios were simulated by changing both material properties and vascular geometrical features to cover both presumed vulnerable and stable plaques. The results were analyzed with respect to lumen gain and wall stresses which are potentially related to the failure of the procedure according to previous studies. Our findings show that an elliptic lumen shape and a thinner fibrous cap with an underlying lipid pool result in higher stenosis reduction, while large calcifications and fibrotic tissue are more prone to recoil. The shielding effect of a thicker fibrous cap helps to reduce local compressive stresses in the soft plaque. The presence of a soft plaque reduces the damage in the healthy vascular structures. Contrarily, the presence of hard plaque promotes less damage volume in the fibrous cap and reduces stress peaks in this region, but they seem to increase stresses in the media-intima layer. Finally the reliability of the achieved results was put into clinical perspective.     

Using in vivo Cine and 3D multi-contrast MRI to determine human atherosclerotic carotid artery material properties and circumferential shrinkage rate and their impact on stress/strain predictions

In vivo magnetic resonance image (MRI)-based computational models have been introduced to calculate atherosclerotic plaque stress and strain conditions for possible rupture predictions. However, patient-specific vessel material properties are lacking in those models, which affects the accuracy of their stress/strain predictions. A noninvasive approach of combining in vivo Cine MRI, multicontrast 3D MRI, and computational modeling was introduced to quantify patient-specific carotid artery material properties and the circumferential shrinkage rate between vessel in vivo and zero-pressure geometries. In vivo Cine and 3D multicontrast MRI carotid plaque data were acquired from 12 patients after informed consent. For each patient, one nearly-circular slice and an iterative procedure were used to quantify parameter values in the modified Mooney-Rivlin model for the vessel and the vessel circumferential shrinkage rate. A sample artery slice with and without a lipid core and three material parameter sets representing stiff, median, and soft materials from our patient data were used to demonstrate the effect of material stiffness and circumferential shrinkage process on stress/strain predictions. Parameter values of the Mooney-Rivlin models for the 12 patients were quantified. The effective Young's modulus (YM, unit: kPa) values varied from 137 (soft), 431 (median), to 1435 (stiff), and corresponding circumferential shrinkages were 32%, 12.6%, and 6%, respectively. Using the sample slice without the lipid core, the maximum plaque stress values (unit: kPa) from the soft and median materials were 153.3 and 96.2, which are 67.7% and 5% higher than that (91.4) from the stiff material, while the maximum plaque strain values from the soft and median materials were 0.71 and 0.293, which are about 700% and 230% higher than that (0.089) from the stiff material, respectively. Without circumferential shrinkages, the maximum plaque stress values (unit: kPa) from the soft, median, and stiff models were inflated to 330.7, 159.2, and 103.6, which were 116%, 65%, and 13% higher than those from models with proper shrinkage. The effective Young's modulus from the 12 human carotid arteries studied varied from 137 kPa to 1435 kPa. The vessel circumferential shrinkage to the zero-pressure condition varied from 6% to 32%. The inclusion of proper shrinkage in models based on in vivo geometry is necessary to avoid over-estimating the stresses and strains by up 100%. Material stiffness had a greater impact on strain (up to 700%) than on stress (up to 70%) predictions. Accurate patient-specific material properties and circumferential shrinkage could considerably improve the accuracy of in vivo MRI-based computational stress/strain predictions.     

Non-uniform shrinkage for obtaining computational start shape for in-vivo MRI-based plaque vulnerability assessment

BackgroundCritical mechanical conditions, such as stress within the structure and shear stress due to blood flow, predicted from in-vivo magnetic resonance image (MRI)-based computational simulations have shown to be potential in assessing carotid plaque vulnerability. Plaque contours obtained from in-vivo MRI are a result of a pressurized configuration due to physiological loading. However, in order to make accurate predictions, the computational model must be based on the loading-free geometry. A shrinkage procedure can be used to obtain the computational start shape.MethodIn this study, electrocardiograph (ECG)-gated MR-images of carotid plaques were obtained from 28 patients. The contours of each plaque were segmented manually. Additional to a uniform shrinkage procedure, a non-uniform shrinkage refinement procedure was used. This procedure was repeated until the pressurized lumen contour and fibrous cap thickness had the best match with the in-vivo image.ResultsCompared to the uniform shrinkage procedure, the non-uniform shrinkage significantly reduced the difference in lumen shape and in cap thickness at the thinnest site. Results indicate that uniform shrinkage would underestimate the critical stress in the structure by 20.5±10.7%.ConclusionFor slices with an irregular lumen shape (the ratio of the maximum width to the minimum width is more than 1.05), the non-uniform shrinkage procedure is needed to get an accurate stress profile for mechanics and MRI-based carotid plaque vulnerability assessment.     

Quantifying effects of plaque structure and material properties on stress distributions in human atherosclerotic plaques using 3D FSI models

BACKGROUND: Atherosclerotic plaques may rupture without warning and cause acute cardiovascular syndromes such as heart attack and stroke. Methods to assess plaque vulnerability noninvasively and predict possible plaque rupture are urgently needed. METHOD: MRI-based three-dimensional unsteady models for human atherosclerotic plaques with multi-component plaque structure and fluid-structure interactions are introduced to perform mechanical analysis for human atherosclerotic plaques. RESULTS: Stress variations on critical sites such as a thin cap in the plaque can be 300% higher than that at other normal sites. Large calcification block considerably changes stress/strain distributions. Stiffness variations of plaque components (50% reduction or 100% increase) may affect maximal stress values by 20-50%. Plaque cap erosion causes almost no change on maximal stress level at the cap, but leads to 50% increase in maximal strain value. CONCLUSIONS: Effects caused by atherosclerotic plaque structure, cap thickness and erosion, material properties, and pulsating pressure conditions on stress/strain distributions in the plaque are quantified by extensive computational case studies and parameter evaluations. Computational mechanical analysis has good potential to improve accuracy of plaque vulnerability assessment.     

Morphological and Stress Vulnerability Indices for Human Coronary Plaques and Their Correlations with Cap Thickness and Lipid Percent: An IVUS-Based Fluid-Structure Interaction Multi-patient Study

Plaque vulnerability, defined as the likelihood that a plaque would rupture, is difficult to quantify due to lack of in vivo plaque rupture data. Morphological and stress-based plaque vulnerability indices were introduced as alternatives to obtain quantitative vulnerability assessment. Correlations between these indices and key plaque features were investigated. In vivo intravascular ultrasound (IVUS) data were acquired from 14 patients and IVUS-based 3D fluid-structure interaction (FSI) coronary plaque models with cyclic bending were constructed to obtain plaque wall stress/strain and flow shear stress for analysis. For the 617 slices from the 14 patients, lipid percentage, min cap thickness, critical plaque wall stress (CPWS), strain (CPWSn) and flow shear stress (CFSS) were recorded, and cap index, lipid index and morphological index were assigned to each slice using methods consistent with American Heart Association (AHA) plaque classification schemes. A stress index was introduced based on CPWS. Linear Mixed-Effects (LME) models were used to analyze the correlations between the mechanical and morphological indices and key morphological factors associated with plaque rupture. Our results indicated that for all 617 slices, CPWS correlated with min cap thickness, cap index, morphological index with r = -0.6414, 0.7852, and 0.7411 respectively (p<0.0001). The correlation between CPWS and lipid percentage, lipid index were weaker (r = 0.2445, r = 0.2338, p<0.0001). Stress index correlated with cap index, lipid index, morphological index positively with r = 0.8185, 0.3067, and 0.7715, respectively, all with p<0.0001. For all 617 slices, the stress index has 66.77% agreement with morphological index. Morphological and stress indices may serve as quantitative plaque vulnerability assessment supported by their strong correlations with morphological features associated with plaque rupture. Differences between the two indices may lead to better plaque assessment schemes when both indices were jointly used with further validations from clinical studies.     

Identification of cholesteryl esters in human carotid atherosclerosis by ex vivo image-guided proton MRS

Vulnerable atherosclerotic plaques may be identified by their large lipid component, particularly liquid cholesteryl ester (CE), covered by a fibrous cap. We hypothesized that image-guided 1H proton magnetic resonance spectroscopy (MRS) would identify mobile CE in discrete, preselected regions of atherosclerotic plaque. Human carotid endarterectomy specimens (n = 10) were imaged ex vivo by magnetic resonance imaging (MRI) at high field (11.7 T) utilizing standard T1- and T2-weighted spin echo protocols. MRS spectra were acquired from 1 mm3 voxels, localized to plaque regions that we judged by MRI to be lipid rich or lipid poor. The spectra revealed methyl and methylene resonances of fatty acyl chains with relative intensities and linewidths characteristic of pure CE, by comparison with lipid standards. Regions judged to be lipid rich by MRI showed much more intense CE resonances than did lipid-poor regions. The integrated intensities of lipid peaks were 5.5 +/- 2.0% (lipid-rich regions) versus 0.9 +/- 0.6% (lipid-poor regions) of the unsuppressed water peak (P < 0.0001). Lipid distribution by histology, MRS, and MRI showed strong correlation. Image-guided proton MRS accurately identified CE in selected regions of atherosclerotic plaque as small as 1 mm3 in an ex vivo setting. This procedure may permit the noninvasive detection and quantification of CE in atherosclerotic plaque in vivo.     

Model-based cap thickness and peak cap stress prediction for carotid MRI

A rupture-prone carotid plaque can potentially be identified by calculating the peak cap stress (PCS). For these calculations, plaque geometry from MRI is often used. Unfortunately, MRI is hampered by a low resolution, leading to an overestimation of cap thickness and an underestimation of PCS. We developed a model to reconstruct the cap based on plaque geometry to better predict cap thickness and PCS.We used histological stained plaques from 34 patients. These plaques were segmented and served as the ground truth. Sections of these plaques contained 93 necrotic cores with a cap thickness <0.62 mm which were used to generate a geometry-based model. The histological data was used to simulate in vivo MRI images, which were manually delineated by three experienced MRI readers. Caps below the MRI resolution (n = 31) were (digitally removed and) reconstructed according to the geometry-based model. Cap thickness and PCS were determined for the ground truth, readers, and reconstructed geometries.Cap thickness was 0.07 mm for the ground truth, 0.23 mm for the readers, and 0.12 mm for the reconstructed geometries. The model predicts cap thickness significantly better than the readers. PCS was 464 kPa for the ground truth, 262 kPa for the readers and 384 kPa for the reconstructed geometries. The model did not predict the PCS significantly better than the readers.The geometry-based model provided a significant improvement for cap thickness estimation and can potentially help in rupture-risk prediction, solely based on cap thickness. Estimation of PCS estimation did not improve, probably due to the complex shape of the plaques.     

Effects of intima stiffness and plaque morphology on peak cap stress

Background  

Rupture of the cap of a vulnerable plaque present in a coronary vessel may cause myocardial infarction and death. Cap rupture occurs when the peak cap stress exceeds the cap strength. The mechanical stress within a cap depends on the plaque morphology and the material characteristics of the plaque components. A parametric study was conducted to assess the effect of intima stiffness and plaque morphology on peak cap stress.     

A mechanistic analysis of the role of microcalcifications in atherosclerotic plaque stability: potential implications for plaque rupture

The role of microcalcifications (μCalcs) in the biomechanics of vulnerable plaque rupture is examined. Our laboratory previously proposed (Ref. 44), using a very limited tissue sample, that μCalcs embedded in the fibrous cap proper could significantly increase cap instability. This study has been greatly expanded. Ninety-two human coronary arteries containing 62 fibroatheroma were examined using high-resolution microcomputed tomography at 6.7-μm resolution and undecalcified histology with special emphasis on calcified particles <50 μm in diameter. Our results reveal the presence of thousands of μCalcs, the vast majority in lipid pools where they are not dangerous. However, 81 μCalcs were also observed in the fibrous caps of nine of the fibroatheroma. All 81 of these μCalcs were analyzed using three-dimensional finite-element analysis, and the results were used to develop important new clinical criteria for cap stability. These criteria include variation of the Young's modulus of the μCalc and surrounding tissue, μCalc size, and clustering. We found that local tissue stress could be increased fivefold when μCalcs were closely spaced, and the peak circumferential stress in the thinnest nonruptured cap (66 μm) if no μCalcs were present was only 107 kPa, far less than the proposed minimum rupture threshold of 300 kPa. These results and histology suggest that there are numerous μCalcs < 15 μm in the caps, not visible at 6.7-μm resolution, and that our failure to find any nonruptured caps between 30 and 66 μm is a strong indication that many of these caps contained μCalcs.     

动脉粥样硬化斑块中脂肪沉积的扫频光热波成像

动脉粥样硬化和易损斑块破裂在全球范围内具有最高的死亡率,超过传染病和癌症导致的死亡率的总和。动脉粥样硬化斑块是由一层很薄的”纤维帽”和导致血栓形成的脂质核心构成。光热波成像是基于对被目标发色团（本文中指脂肪沉积）吸收的光信号强度进行周期调制,从而实现对目标发色团释放的热（红外）信号的调制。这里,我们利用光热波成像来检测来自兔子动脉硬化模型的粥样硬化斑块中脂肪沉积的三维分布。波长为1210纳米的激光被用来靶向检测脂肪。动脉粥样硬化斑块组织在0．1到5赫兹连续扫频的激光的激发下发出光热波,光热波传播到样品表面形成红外辐射温度并被红外相机以25．6帧／秒的速度接收并录制20秒。红外相机上的每一个像素（总共256~256像素）在进行时域傅里叶变换以后得到强度和相位的频域光热波图像。某一特定频率的强度和相位光热波图像对应着脂肪沉积在动脉粥样硬化斑块样品中的横向和纵向分布。对强度和相位光热波图像的分析指出：光热波成像能够用来检测脂肪在动脉粥样硬化斑块中的三维分布,并且脂肪的分布和动脉粥样硬化斑块的形状特征有着紧密联系。     

Stress-Based Plaque Vulnerability Index and Assessment for Carotid Atherosclerotic Plaques Using Patient-Specific Vessel Material Properties

Cardiovascular diseases are closely linked to atherosclerotic plaque development and rupture. Assessment of plaque vulnerability is of fundamental significance to cardiovascular research and disease diagnosis, prevention, treatment and management. Magnetic resonance image (MRI) data of carotid atherosclerotic plaques from 8 patients (5 male, 3 female; age: 62-83, mean=71) were acquired at the University of Washington (UW), Seattle by the Vascular Imaging Laboratory (VIL) with written informed consent obtained. Patient-specific vessel material properties were quantified using Cine MRI data for modeling use. 3D thin-layer models were used to obtain plaque stress and strain for plaque assessment. A stress-based plaque vulnerability index (SPVI) was proposed to combine mechanical analysis, plaque morphology and composition for more complete carotid plaque vulnerability assessment. The five intervals (unit: kPa) [0, 46.8), [46.8, 80), [80, 92), [92, 103), and [103, +∞) from in vivo material models were used for SPVI values of 0, 1, 2, 3 and 4, respectively. The optimized agreement rate was 85.19%. The use of patient-specific material properties in plaque models could potentially improve the accuracy of model stress/strain calculations. SPVI has the potential to improve the current image-based screening and plaque vulnerability assessment schemes.