Quantifying Effects of Artery Shrinkage Using In Vivo MRI-Based 3D FSI Models for Carotid Atherosclerotic Plaques With Bifurcation

Author(s):  
Xueying Huang ◽  
Chun Yang ◽  
Chun Yuan ◽  
Thomas Hatsukami ◽  
Fei Liu ◽  
...  

Atherosclerotic vascular disease leads to changes of the arterial wall and lumen narrowing, and it is the No.1 killer in the western world. Magnetic resonance image (MRI)-based computational models with fluid-structure interactions (FSI) for atherosclerotic plaques have been introduced to perform mechanical analysis to quantify critical flow and stress/strain conditions related to plaque rupture which often leads directly to heart attack or stroke [2]. There are three groups of information needed as model input: plaque morphology, material properties, and flow conditions. Pre shrinkage-stretch process is used to recover the in vivo geometry from zero-stress state with associated initial conditions which are required to achieve building the computational model. An important issue for this process is how to determine zero stress state from in vivo plaque geometry. However, few publications can be found in the current literature about how to quantify human carotid artery shrinkage.

2016 ◽  
Vol 6 (1) ◽  
pp. 20150044 ◽  
Author(s):  
Fei Fang ◽  
Spencer P. Lake

Tendon exhibits anisotropic, inhomogeneous and viscoelastic mechanical properties that are determined by its complicated hierarchical structure and varying amounts/organization of different tissue constituents. Although extensive research has been conducted to use modelling approaches to interpret tendon structure–function relationships in combination with experimental data, many issues remain unclear (i.e. the role of minor components such as decorin, aggrecan and elastin), and the integration of mechanical analysis across different length scales has not been well applied to explore stress or strain transfer from macro- to microscale. This review outlines mathematical and computational models that have been used to understand tendon mechanics at different scales of the hierarchical organization. Model representations at the molecular, fibril and tissue levels are discussed, including formulations that follow phenomenological and microstructural approaches (which include evaluations of crimp, helical structure and the interaction between collagen fibrils and proteoglycans). Multiscale modelling approaches incorporating tendon features are suggested to be an advantageous methodology to understand further the physiological mechanical response of tendon and corresponding adaptation of properties owing to unique in vivo loading environments.


Author(s):  
Zheyang Wu ◽  
Chun Yang ◽  
Dalin Tang

It has been hypothesized that mechanical risk factors may be used to predict future atherosclerotic plaque rupture. Much progress has been made in computational modeling, medical imaging, and mechanical analysis for atherosclerotic plaque vulnerability assessment in recent years [1–2]. However, truly predictive methods to predict plaque rupture are currently lacking in the literature and practice. In this paper, we introduce a procedure using computational and statistical models based on serial magnetic resonance imaging (MRI) to quantify sensitivity and specificity of mechanical predictors and their combinations to identify the best candidate for rupture prediction. Serial MRI of carotid plaque from a patient with follow-up scan showing ulceration (rupture) was acquired and the actual appearance of ulceration was used as “gold standard” and validation for the predictive method.


Author(s):  
Renate W. Boekhoven ◽  
Marcel C. M. Rutten ◽  
Marc R. H. M. van Sambeek ◽  
Frans N. van de Vosse ◽  
Richard G. P. Lopata

Treatment of rupture-prone carotid atherosclerotic plaques, by means of endarterectomy, is only beneficial for patients with unstable plaques, which comprise only 16% of the patient population [1]. It is therefore of great interest to assess morphology, geometry and mechanical deformation of the plaque and its components, to prevent unnecessary treatment. However, due to the complex geometry of stenotic arteries, 3D information at both high temporal and spatial resolution is required. Besides, assessment of plaque morphology in vivo can still not be routinely performed. Therefore, one has to rely on in vitro methods to obtain morphology and mechanical properties, and thus rupture risk.


2005 ◽  
Vol 127 (7) ◽  
pp. 1185-1194 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
Jeffrey E. Saffitz ◽  
...  

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.


2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Jason L. Johnson ◽  
Nicholas P. Jenkins ◽  
Wei-Chun Huang ◽  
Karina Di Gregoli ◽  
Graciela B. Sala-Newby ◽  
...  

Matrix metalloproteinase-14 (MMP-14) promotes vulnerable plaque morphology in mice, whereas tissue inhibitor of metalloproteinases-3 (TIMP-3) overexpression is protective.MMP-14hi  TIMP-3lorabbit foam cells are more invasive and more prone to apoptosis thanMMP-14lo  TIMP-3hicells. We investigated the implications of these findings for human atherosclerosis.In vitrogenerated macrophages and foam-cell macrophages, together with atherosclerotic plaques characterised as unstable or stable, were examined for expression of MMP-14, TIMP-3, and inflammatory markers. Proinflammatory stimuli increased MMP-14 and decreased TIMP-3 mRNA and protein expression in human macrophages. However, conversion to foam-cells with oxidized LDL increased MMP-14 and decreased TIMP-3 protein, independently of inflammatory mediators and partly through posttranscriptional mechanisms. Within atherosclerotic plaques, MMP-14 was prominent in foam-cells with either pro- or anti-inflammatory macrophage markers, whereas TIMP-3 was present in less foamy macrophages and colocalised with CD206. MMP-14 positive macrophages were more abundant whereas TIMP-3 positive macrophages were less abundant in plaques histologically designated as rupture prone. We conclude that foam-cells characterised by high MMP-14 and low TIMP-3 expression are prevalent in rupture-prone atherosclerotic plaques, independent of pro- or anti-inflammatory activation. Therefore reducing MMP-14 activity and increasing that of TIMP-3 could be valid therapeutic approaches to reduce plaque rupture and myocardial infarction.


Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
Kristen Billiar ◽  
...  

Assessing atherosclerotic plaque vulnerability based on limited in vivo patient data has been a major challenge in cardiovascular research and clinical practice. Considerable advances in medical imaging technology have been made in recent years to identify vulnerable atherosclerotic carotid plaques in vivo with information about plaque components including lipid-rich necrotic pools, calcification, intraplaque hemorrhage, loose matrix, thrombosis, and ulcers, subject to resolution limitations of current technology [1]. Image-based computational models have also been developed which combine mechanical analysis with image technology aiming for more accurate assessment of plaque vulnerability and better diagnostic and treatment decisions [2]. However, 3D models with fluid-structure interactions (FSI), cyclic bending and anisotropic properties based on in vivo IVUS images for human coronary atherosclerotic plaques are lacking in the current literature. In this paper, we introduce 3D FSI models based on in vivo IVUS images to perform mechanical analysis for human coronary plaques. Cyclic bending is included to represent deformation caused by cardiac motion. An anisotropic material model was used for the vessel so that the models would be more realistic for more accurate computational flow and stress/strain predictions.


Author(s):  
Krishna Prasad ◽  
Sreeniavs Reddy S ◽  
Jaspreet Kaur ◽  
Raghavendra Rao k ◽  
Suraj Kumar ◽  
...  

Introduction: Women perform worse after acute coronary syndrome (ACS) than men. The reason for these differences is unclear. The aim was to ascertain gender differences in the culprit plaque characteristics in ACS. Methods:Patients with ACS undergoing percutaneous coronary intervention for the culprit vessel underwent optical coherence tomography (OCT) imaging. Culprit plaque was identified as lipid rich,fibrous, and calcific plaque. Mechanisms underlying ACS are classified as plaque rupture, erosion,or calcified nodule. A lipid rich plaque along with thin-cap fibroatheroma (TCFA) was a vulnerable plaque. Plaque microstructures including cholesterol crystals, macrophages, and microvessels were noted. Results: A total of 52 patients were enrolled (men=29 and women=23). Baseline demographic features were similar in both the groups except men largely were current smokers (P<0.001). Plaque morphology,men vs. women: lipid rich 88.0% vs. 90.5%; fibrous 4% vs 0%; calcific 8.0% vs. 9.5% (P = 0.64). Of the ACS mechanisms in males versus females; plaque rupture (76.9 % vs. 50 %), plaque erosion (15.4 % vs.40 %) and calcified nodule (7.7 % vs. 10 %) was noted (P = 0.139). Fibrous cap thickness was (50.19 ±11.17 vs. 49.00 ± 10.71 mm, P = 0.71) and thin-cap fibroatheroma (96.2% vs. 95.0%, P = 1.0) in men and women respectively. Likewise no significant difference in presence of macrophages (42.3 % vs. 30%, P = 0.76), microvessels (73.1% vs. 60 %, P = 0.52) and cholesterol crystals (92.3% vs. 80%, P = 0.38). Conclusion: No significant gender-based in-vivo differences could be discerned in ACS patients’ culprit plaques morphology, characteristics, and underlying mechanisms.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takashi Kubo ◽  
Akiko Maehara ◽  
Gary S Mintz ◽  
Hiroshi Doi ◽  
Kenichi Tsujita ◽  
...  

Thin-cap fibroatheromas (TCFA) are prone to plaque rupture and thrombosis. Intravascular ultrasound (IVUS) virtual histology (VH) assesses plaque composition and lesion morphology in vivo. Methods & Results: We used serial (baseline and follow-up @11 mos) VH-IVUS to study non-culprit plaque morphology in 221 lesions (plaque burden >40%) in 106 pts. Lesions were classified into 4 types based on plaque composition; pathological intimal thickening (PIT), thin-capped fibroatheroma (TCFA), thick-capped fibroatheroma (ThCFA), fibrotic/fibrocalcific. At baseline, 21 lesions were TCFAs (confluent necrotic core contacting to the lumen). Overall during follow-up (Figure ), 16/21 (76%) TCFAs healed: 13 became ThCFAs, 2 TCFAs became PIT, 1 TCFA became fibrotic, and 5 TCFAs (24%) remains unchanged although the location of the necrotic core in contact with the lumen shifted axially. Compared to TCFAs that healed, TCFAs that remained TCFAs were more often proximal in location (distance from coronary ostium to the lesion of 19±6 vs. 41±22mm, respectively, p=0.037) and had larger lumen area (9.9±3.1 vs. 6.9±1.8 mm2, p=0.013), vessel area (22.8±6.4 vs. 15.3±2.6 mm2, p=0.001), plaque area (12.9±4.9 vs. 8.4±1.7 mm2, p=0.005), calcium area (1.3±0.6 vs. 0.6±0.3 mm2, p=0.014), and necrotic core area (2.6±1.0 vs. 1.6±0.7 mm2, p=0.015). In addition, 6 new TCFAs developed; these 6 late-developing TCFAs had the appearance of PIT at baseline (Figure ). Conclusion: Although most TCFAs seem to stabilize or heal during 12 mos follow-up, proximal TCFAs in larger vessels with more plaque and calcium and a larger necrotic core appear to heal less often and new TCFAs can develop.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sining Hu ◽  
Haibo Jia ◽  
Tsunenari Soeda ◽  
Yoshiyasu Minami ◽  
Rocco Vergallo ◽  
...  

Introduction: Autopsy studies in sudden cardiac death subjects showed female had higher incidence of erosion. However, the incidence of erosion in patients with acute myocardial infarction (AMI) has not been systematically studied. Hypothesis: This study was to study the gender difference in the prevalence and morphological characteristics of the culprit lesion in patients with AMI using intravascular optical coherence tomography (OCT). Methods: A total of 79 patients (65 male and 14 female) with AMI who underwent pre-intervention OCT imaging of the culprit lesion were included. Results: Baseline characteristics between the two groups were similar. In OCT findings, the incidence of thin-cap fibroatheroma (TCFA) was slightly lower and the fibrous cap thickness was slightly thicker in female than in male, but the differences were not significant. Defining underlying plaque morphology by genders, plaque erosion was more prevalent in female than in male, whereas plaque rupture was more frequent in male (Table). Conclusions: Erosion was the most frequent cause of AMI in female patients, whereas plaque rupture is the predominant underlying pathology of AMI in male patients.


Author(s):  
Xueying Huang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Richard Bach ◽  
David Muccigrosso ◽  
...  

Atherosclerotic plaque rupture is the primary cause of cardiovascular clinical events such as heart attack and stroke. It is commonly believed that plaque rupture may be linked to critical mechanical conditions. Image-based computational models of vulnerable plaques have been introduced seeking critical mechanical indicators which may be used to identify potential sites of rupture [1–5]. A recent study by Tang et al. [4] using in vivo MRI-based 3D fluid-structure interaction (FSI) models for human carotid plaques with and without rupture reported that higher critical plaque wall stress (CPWS) values were associated with plaques with rupture, compared to those without rupture. However, existing computational plaque models are mostly for carotid plaques based on MRI data. Comparable similar studies for coronary plaques are lacking in the current literature. In this study, 3D computational multi-component models with FSI were constructed to identified 3D critical plaque wall stress, critical flow shear stress (CFSS) based on ex vivo MRI data of coronary plaques acquired from 10 patients. The patients were split into 2 groups: patients died in carotid artery disease (CAD, Group 1, 6 patients) and non CAD (Group 2, 4 patients). The possible link between CPWS and death in CAD was investigated by comparing the CPWS values from the two groups.


Sign in / Sign up

Export Citation Format

Share Document