Sudden Death in Coronary Artery Disease are Associated With High 3D Critical Plaque Wall Stress: A 3D Multi-Patient FSI Study Based on Ex Vivo MRI of Coronary Plaques

2013 ◽  
Author(s):  
Xueying Huang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Richard Bach ◽  
David Muccigrosso ◽  
...  
Keyword(s):  
Computational Models ◽  
Plaque Rupture ◽  
Ex Vivo ◽  
Carotid Artery Disease ◽  
Wall Stress ◽  
Carotid Plaques ◽  
Group 2 ◽  
Artery Disease ◽  
Atherosclerotic Plaque Rupture

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.

scholarly journals 3D Critical Plaque Wall Stress Is a Better Predictor of Carotid Plaque Rupture Sites Than Flow Shear Stress: An In Vivo MRI-Based 3D FSI Study

2010 ◽  
Vol 132 (3) ◽  
Author(s):  
Zhongzhao Teng ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Chun Yang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Plaque Rupture ◽  
Wall Stress ◽  
Flow Shear ◽  
Flow Shear Stress ◽  
The Mean ◽  
Group 2 ◽  
Atherosclerotic Plaque Rupture ◽  
Group 1

Atherosclerotic plaque rupture leading to stroke is the major cause of long-term disability as well as the third most common cause of mortality. Image-based computational models have been introduced seeking critical mechanical indicators, which may be used for plaque vulnerability assessment. This study extends the previous 2D critical stress concept to 3D by using in vivo magnetic resonance image (MRI) data of human atherosclerotic carotid plaques and 3D fluid-structure interaction (FSI) models to: identify 3D critical plaque wall stress (CPWS) and critical flow shear stress (CFSS) and to investigate their associations with plaque rupture. In vivo MRI data of carotid plaques from 18 patients scheduled for endarterectomy were acquired using histologically validated multicontrast protocols. Of the 18 plaques, histology-confirmed that six had prior rupture (group 1) as evidenced by presence of ulceration. The remaining 12 plaques (group 2) contained no rupture. The 3D multicomponent FSI models were constructed for each plaque to obtain 3D plaque wall stress (PWS) and flow shear stress (FSS) distributions. Three-dimensional CPWS and CFSS, defined as maxima of PWS and FSS from all vulnerable sites, were determined for each plaque to investigate their association with plaque rupture. Slice-based critical PWS and FSS were also calculated for all slices for more detailed analysis and comparison. The mean 3D CPWS of group 1 was 263.44 kPa, which was 100% higher than that from group 2 (132.77, p=0.03984). Five of the six ruptured plaques had 3D CPWS sites, matching the histology-confirmed rupture sites with an 83% agreement. Although the mean 3D CFSS (92.94 dyn/cm2) for group 1 was 76% higher than that for group 2 (52.70 dyn/cm2), slice-based CFSS showed no significant difference between the two groups. Only two of the six ruptured plaques had 3D CFSS sites matching the histology-confirmed rupture sites with a 33% agreement. CFSS had a good correlation with plaque stenosis severity (R2=0.40 with an exponential function fitting 3D CFSS data). This in vivo MRI pilot study using plaques with and without rupture demonstrates that 3D critical plaque wall stress values are more closely associated with atherosclerotic plaque rupture then critical flow shear stresses. Critical wall stress values may become indicators of high risk sites of rupture. Future work with a larger population will establish a possible CPWS-based plaque vulnerability classification.

Predicting Human Carotid Plaque Site of Rupture Using 3D Critical Plaque Wall Stress and Flow Shear Stress: A 3D Multi-Patient FSI Study Based on In Vivo MRI of Plaques With and Without Prior Rupture

2010 ◽  
Author(s):  
Zhongzhao Teng ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Chun Yang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Critical Stress ◽  
Plaque Rupture ◽  
Wall Stress ◽  
Global Maximum ◽  
Flow Shear ◽  
Carotid Plaques ◽  
Flow Shear Stress ◽  
Human Carotid

Atherosclerotic plaque rupture is the primary cause of cardiovascular clinical events such as heart attack and stroke. 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]. Models derived from 2D ex vivo and in vivo magnetic resonance images (MRI) have shown that 2D local critical stress values rather than global maximum stress values correlated better with plaque vulnerability, as defined by histopathological and morphological analyses [5]. A recent study by Tang et al. [4] using in vivo MRI-based 3D fluid-structure interaction (FSI) models for ruptured human carotid plaques, reported that mean plaque wall stress (PWS) values from ulcer nodes were 86% higher than mean PWS values from all non-ulcer nodes (p<0.0001). This study extends the “critical stress” concept to 3D and uses 3D FSI models based on in vivo MRI data of human atherosclerotic carotid plaques with and without prior rupture to identify 3D critical plaque wall stress (CPWS), critical flow shear stress (CFSS), and to investigate their associations with plaque rupture.

scholarly journals Imaging of nonatheromatous carotid artery disease

2021 ◽  
Vol 5 (1) ◽  
pp. 2514183X2110145
Author(s):  
Daniel Montes ◽  
Javier M Romero
Keyword(s):  
Carotid Artery ◽  
Plaque Rupture ◽  
Carotid Artery Disease ◽  
Imaging Features ◽  
Imaging Evaluation ◽  
Inflammatory Conditions ◽  
Risk Patients ◽  
Artery Disease ◽  
Low Prevalence ◽  
Atherosclerotic Plaque Rupture

Imaging diagnosis of nonatheromatous carotid artery disease is challenging due to its low prevalence in contrast to that of atheromatous disease. Congenital anomalies are frequently discovered incidentally, as the chronicity of these conditions allows for compensatory flow development. The inflammatory conditions typically present with nonspecific courses, and a high clinical suspicion along with timely imaging evaluation can guide the diagnosis. Carotid dissection is the result of a partial disruption of the arterial wall and can be seen in previously healthy patients, in patients with underlying noninflammatory arteriopathies or trauma. Traumatic injuries to the carotid artery may occur under many different conditions and mechanisms and timely recognition of high-risk patients improves patient outcomes. Although free-floating thrombi (FFT) formation is typically seen with atherosclerotic plaque rupture, different conditions may also predispose to FFT. In this review article, we study the different imaging features of nonatheromatous carotid artery disease using ultrasonography, computed tomography angiography, magnetic resonance angiography, and digital subtraction angiogram.

A Framework to Assess Human Coronary Plaque Vulnerability Using Intravascular Ultrasound, On-Site Pressure, Angiography, and Anisotropic FSI Models

2012 ◽  
Author(s):  
Haofei Liu ◽  
Mingchao Cai ◽  
Chun Yang ◽  
Jie Zheng ◽  
Richard Bach ◽  
...  
Keyword(s):  
Intravascular Ultrasound ◽  
Computational Models ◽  
Plaque Rupture ◽  
Coronary Plaque ◽  
Critical Flow ◽  
Stress Strain ◽  
Flow Measurements ◽  
Biaxial Mechanical Testing ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture is believed to be associated with critical flow and stress/strain conditions. Image-based computational models have been developed to identify critical flow and stress/strain conditions in the plaque [1–3]. In vivo image-based coronary plaque modeling papers are relatively rare because clinical recognition of vulnerable coronary plaques has remained challenging [4]. In this paper, a framework adopting intravascular ultrasound (IVUS) imaging with on-site pressure and flow measurements, biaxial mechanical testing and computational modeling is proposed to construct 3D coronary plaque for more accurate stress/strain predictions.

Influence of SIN-1 on Platelet Ca2+ Handling in Patients with Suspected Coronary Artery Disease: Ex Vivo and In Vitro Studies

2000 ◽  
Vol 83 (05) ◽  
pp. 752-758 ◽  
Author(s):  
Claude Le Feuvre ◽  
Annie Brunet ◽  
Thuc Do Pham ◽  
Jean-Philippe Metzger ◽  
André Vacheron ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Vascular Tone ◽  
Ex Vivo ◽  
Suspected Coronary Artery Disease ◽  
In Vitro Studies ◽  
H2o2 Formation ◽  
Artery Disease ◽  
Dose Dependent

SummaryThe 3-morpholinosydnonimine (SIN-1) generates both nitric oxide (NO) and superoxide anion (O2−). It elicits dose-dependent vasodilation in vivo, in spite of the opposite effects of its breakdown products on vascular tone and platelet aggregation.This study was designed to investigate the influence of intravenous SIN-1 injection on platelet Ca2+ handling in patients undergoing coronary angiography. SIN-1 administration reduced cytosolic [Ca2+] in unstimulated platelets by decreasing Ca2+ influx. It attenuated Ca2+ mobilization from internal stores evoked by thrombin or thapsigargin. In vitro studies were used as an approach to investigate how simultaneous productions of NO and O2− from SIN-1 modify thrombin- or thapsigargin-induced platelet Ca2+ mobilization. Superoxide dismutase, the O2− scavenger, enhanced the capacity of SIN-1 to inhibit Ca2+ mobilization but catalase had no effect.This suggests that the effects of SIN-1 on platelet Ca2+ handling resemble those of NO, but are modulated by simultaneous O2− release, independently of H2O2 formation.

A New Hypothesis for Human Atherosclerotic Plaque Progression Based on Serial In Vivo MRI and Computational Modeling Method

2007 ◽  
Author(s):  
Sayan Mondal ◽  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Chun Yuan ◽  
Fei Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Thickness ◽  
Computational Models ◽  
Ex Vivo ◽  
Maximum Principal Stress ◽  
Magnetic Resonance Images ◽  
Shear Stresses ◽  
Flow Shear ◽  
Flow Shear Stress

It has been well-accepted that atherosclerosis initiation and progression correlate positively with low and oscillating flow wall shear stresses. However, this shear stress mechanism cannot fully explain why advanced plaques continue to grow under elevated flow shear stress conditions. Our previous investigations using 3D computational models with fluid-structure interactions (FSI) based on in vivo/ex vivo magnetic resonance images (MRI) of human carotid atherosclerotic plaques indicated that there is a negative correlation between advanced plaque wall thickness and structural maximum principal stress (Stress-P1) in the plaque and a positive correlation between plaque wall thickness and flow shear stress [3].

Reversed Correlations Between Atherosclerotic Carotid Plaque Progression and Flow Shear Stress/Plaque Wall Stress Based on Past and Current Scan Data: In Vivo MRI-Based 3D FSI Studies

2010 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Thomas Hatsukami ◽  
Dalin Tang
Keyword(s):  
Shear Stress ◽  
Wall Stress ◽  
Significant Negative Correlation ◽  
Shear Stresses ◽  
Plaque Progression ◽  
Flow Shear ◽  
Carotid Plaques ◽  
Flow Shear Stress ◽  
The Difference

It has been well accepted that low and oscillating blood flow shear stresses (LFSS) correlate positively with intimal thickening and atherosclerosis initiation [1,2]. However, the LFSS hypothesis cannot explain why advanced plaques continue to grow under elevated high flow shear stress conditions [3]. For patient tracking studies, plaque progression is often measured by the difference of plaque geometries between two scans (“past” and “current” scans) when medical imaging is used. Mechanical flow shear stress (FSS) and plaque wall stress (PWS) conditions from the two scans may have different correlations with plaque progression. Using 2D structure models based on in vivo magnetic resonance imaging (MRI) human carotid plaques, Tang et al. showed that 18 out of 21 patients had significant negative correlation between plaque progression measured by wall thickness increase (WTI) and plaque wall stress from current scan [3]. The correlation was reversed when plaque wall stress from past scan was used. In this paper, 3D fluid-structure interactions (FSI) models for 32 matched “past-current” scan pairs of human atherosclerotic carotid plaques based on in vivo MRI data were solved and plaque wall stress (PWS) and flow shear stress (FSS) data were obtained to quantify their correlations with plaque progression measured by WTI.

scholarly journals Models of tendon development and injury

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Sophia K. Theodossiou ◽  
Nathan R. Schiele
Keyword(s):  
Computational Models ◽  
Ex Vivo ◽  
Current Model ◽  
Stem Cell Differentiation ◽  
Tendon Injury ◽  
Model Systems ◽  
Tendon Development ◽  
Key Aspects

AbstractTendons link muscle to bone and transfer forces necessary for normal movement. Tendon injuries can be debilitating and their intrinsic healing potential is limited. These challenges have motivated the development of model systems to study the factors that regulate tendon formation and tendon injury. Recent advances in understanding of embryonic and postnatal tendon formation have inspired approaches that aimed to mimic key aspects of tendon development. Model systems have also been developed to explore factors that regulate tendon injury and healing. We highlight current model systems that explore developmentally inspired cellular, mechanical, and biochemical factors in tendon formation and tenogenic stem cell differentiation. Next, we discuss in vivo, in vitro, ex vivo, and computational models of tendon injury that examine how mechanical loading and biochemical factors contribute to tendon pathologies and healing. These tendon development and injury models show promise for identifying the factors guiding tendon formation and tendon pathologies, and will ultimately improve regenerative tissue engineering strategies and clinical outcomes.

scholarly journals Fluid Structural Analysis of Urine Flow in a Stented Ureter

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
J. Carlos Gómez-Blanco ◽  
F. Javier Martínez-Reina ◽  
Domingo Cruz ◽  
J. Blas Pagador ◽  
Francisco M. Sánchez-Margallo ◽  
...  
Keyword(s):  
Computational Models ◽  
Mechanical Characterization ◽  
Ex Vivo ◽  
Biological Tissues ◽  
Urine Flow ◽  
Computational Environment ◽  
Computational Fluid Dynamics Cfd

Many urologists are currently studying new designs of ureteral stents to improve the quality of their operations and the subsequent recovery of the patient. In order to help during this design process, many computational models have been developed to simulate the behaviour of different biological tissues and provide a realistic computational environment to evaluate the stents. However, due to the high complexity of the involved tissues, they usually introduce simplifications to make these models less computationally demanding. In this study, the interaction between urine flow and a double-J stented ureter with a simplified geometry has been analysed. The Fluid-Structure Interaction (FSI) of urine and the ureteral wall was studied using three models for the solid domain: Mooney-Rivlin, Yeoh, and Ogden. The ureter was assumed to be quasi-incompressible and isotropic. Data obtained in previous studies from ex vivo and in vivo mechanical characterization of different ureters were used to fit the mentioned models. The results show that the interaction between the stented ureter and urine is negligible. Therefore, we can conclude that this type of models does not need to include the FSI and could be solved quite accurately assuming that the ureter is a rigid body and, thus, using the more simple Computational Fluid Dynamics (CFD) approach.

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