Translational Application of In Vivo Imaging and Analysis of Atherosclerotic Plaque Vulnerability Assessment

2013 ◽  
Vol 3 (1) ◽  
pp. 14-26
Author(s):  
Kiyoko Uno ◽  
Yu Kataoka ◽  
Rishi Puri ◽  
Stephen J. Nicholls
Author(s):  
Gerard T. Luk-Pat ◽  
Garry E. Gold ◽  
Eric W. Olcott ◽  
Bob S. Hu ◽  
Dwight G. Nishimura

Author(s):  
Zhongzhao Teng ◽  
Xueying Huang ◽  
Chun Yuan ◽  
Gador Canton ◽  
Fei Liu ◽  
...  

Carotid atherosclerotic plaque (CAP) may rupture without warning and cause acute cardiovascular syndromes such as stroke, which is the No.3 killer in USA and a leading cause of serious disabilities. Available screening and diagnosis techniques are insufficient to identify those victims before the event occurs. Noninvasive methods to identify new and emerging biomarkers to assess plaque vulnerability and predict possible rupture before the fatal event are urgently called for.


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.


2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Jin-Ling Ren ◽  
Yao Chen ◽  
Lin-Shuang Zhang ◽  
Ya-Rong Zhang ◽  
Shi-Meng Liu ◽  
...  

AbstractAtherosclerotic plaque vulnerability and rupture increase the risk of acute coronary syndromes. Advanced lesion macrophage apoptosis plays important role in the rupture of atherosclerotic plaque, and endoplasmic reticulum stress (ERS) has been proved to be a key mechanism of macrophage apoptosis. Intermedin (IMD) is a regulator of ERS. Here, we investigated whether IMD enhances atherosclerotic plaque stability by inhibiting ERS-CHOP-mediated apoptosis and subsequent inflammasome in macrophages. We studied the effects of IMD on features of plaque vulnerability in hyperlipemia apolipoprotein E-deficient (ApoE−/−) mice. Six-week IMD1-53 infusion significantly reduced atherosclerotic lesion size. Of note, IMD1-53 lowered lesion macrophage content and necrotic core size and increased fibrous cap thickness and vascular smooth muscle cells (VSMCs) content thus reducing overall plaque vulnerability. Immunohistochemical analysis indicated that IMD1-53 administration prevented ERS activation in aortic lesions of ApoE−/− mice, which was further confirmed in oxidized low-density lipoproteins (ox-LDL) induced macrophages. Similar to IMD, taurine (Tau), a non-selective ERS inhibitor significantly reduced atherosclerotic lesion size and plaque vulnerability. Moreover, C/EBP-homologous protein (CHOP), a pro-apoptosis transcription factor involved in ERS, was significantly increased in advanced lesion macrophages, and deficiency of CHOP stabilized atherosclerotic plaques in AopE−/− mice. IMD1-53 decreased CHOP level and apoptosis in vivo and in macrophages treated with ox-LDL. In addition, IMD1-53 infusion ameliorated NLRP3 inflammasome and subsequent proinflammatory cytokines in vivo and in vitro. IMD may attenuate the progression of atherosclerotic lesions and plaque vulnerability by inhibiting ERS-CHOP-mediated macrophage apoptosis, and subsequent NLRP3 triggered inflammation. The inhibitory effect of IMD on ERS-induced macrophages apoptosis was probably mediated by blocking CHOP activation.


2009 ◽  
Vol 131 (6) ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Shunichi Kobayashi ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
...  

Heart attack and stroke are often caused by atherosclerotic plaque rupture, which happens without warning most of the time. Magnetic resonance imaging (MRI)-based atherosclerotic plaque models with fluid-structure interactions (FSIs) have been introduced to perform flow and stress/strain analysis and identify possible mechanical and morphological indices for accurate plaque vulnerability assessment. For coronary arteries, cyclic bending associated with heart motion and anisotropy of the vessel walls may have significant influence on flow and stress/strain distributions in the plaque. FSI models with cyclic bending and anisotropic vessel properties for coronary plaques are lacking in the current literature. In this paper, cyclic bending and anisotropic vessel properties were added to 3D FSI coronary plaque models so that the models would be more realistic for more accurate computational flow and stress/strain predictions. Six computational models using one ex vivo MRI human coronary plaque specimen data were constructed to assess the effects of cyclic bending, anisotropic vessel properties, pulsating pressure, plaque structure, and axial stretch on plaque stress/strain distributions. Our results indicate that cyclic bending and anisotropic properties may cause 50–800% increase in maximum principal stress (Stress-P1) values at selected locations. The stress increase varies with location and is higher when bending is coupled with axial stretch, nonsmooth plaque structure, and resonant pressure conditions (zero phase angle shift). Effects of cyclic bending on flow behaviors are more modest (9.8% decrease in maximum velocity, 2.5% decrease in flow rate, 15% increase in maximum flow shear stress). Inclusion of cyclic bending, anisotropic vessel material properties, accurate plaque structure, and axial stretch in computational FSI models should lead to a considerable improvement of accuracy of computational stress/strain predictions for coronary plaque vulnerability assessment. Further studies incorporating additional mechanical property data and in vivo MRI data are needed to obtain more complete and accurate knowledge about flow and stress/strain behaviors in coronary plaques and to identify critical indicators for better plaque assessment and possible rupture predictions.


2011 ◽  
Vol 44 (12) ◽  
pp. 2316-2319 ◽  
Author(s):  
Yuan Huang ◽  
Zhongzhao Teng ◽  
Umar Sadat ◽  
Sarah Hilborne ◽  
Victoria E. Young ◽  
...  

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