scholarly journals Local critical stress correlates better than global maximum stress with plaque morphological features linked to atherosclerotic plaque vulnerability: an in vivo multi-patient study

2009 ◽  
Vol 8 (1) ◽  
pp. 15 ◽  
Author(s):  
Dalin Tang ◽  
Zhongzhao Teng ◽  
Gador Canton ◽  
Thomas S Hatsukami ◽  
Li Dong ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Critical Stress ◽  
Maximum Stress ◽  
Morphological Features ◽  
Global Maximum ◽  
Plaque Vulnerability ◽  
Patient Study ◽  
Better Than

Computational Plaque Vulnerability Index for Atherosclerotic Carotid Plaque Assessment Based on In Vivo MR-Image

2008 ◽  
Author(s):  
Zhongzhao Teng ◽  
Xueying Huang ◽  
Chun Yuan ◽  
Gador Canton ◽  
Fei Liu ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Carotid Plaque ◽  
Vulnerability Index ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Vulnerability ◽  
Mr Image ◽  
Noninvasive Methods ◽  
Screening And Diagnosis

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.

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.

3D In Vivo IVUS-Based Anisotropic FSI Models With Cyclic Bending for Human Coronary Atherosclerotic Plaque Mechanical Analysis

2009 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
Kristen Billiar ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Computational Models ◽  
Material Model ◽  
3D Models ◽  
Mechanical Analysis ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Cardiovascular Research ◽  
Cyclic Bending

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.

scholarly journals Intermedin1-53 attenuates atherosclerotic plaque vulnerability by inhibiting CHOP-mediated apoptosis and inflammasome in macrophages

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Jin-Ling Ren ◽  
Yao Chen ◽  
Lin-Shuang Zhang ◽  
Ya-Rong Zhang ◽  
Shi-Meng Liu ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Atherosclerotic Lesion ◽  
Immunohistochemical Analysis ◽  
Inhibitory Effect ◽  
Lesion Size ◽  
Plaque Vulnerability ◽  
Macrophage Apoptosis ◽  
Advanced Lesion

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.

Atherosclerotic Carotid Plaques With Prior Rupture Are Associated With Higher Structural Stresses: In Vivo MRI-Based 3D FSI Studies

2009 ◽  
Author(s):  
Zhongzhao Teng ◽  
Joseph D. Petruccelli ◽  
Xueying Huang ◽  
Chun Yang ◽  
Zijie Liao ◽  
...  
Keyword(s):  
Gold Standard ◽  
Critical Stress ◽  
Plaque Rupture ◽  
Image Data ◽  
Plaque Vulnerability ◽  
Current Image ◽  
Prevention And Treatment ◽  
Assessment Techniques ◽  
Structural Stresses

Atherosclerotic plaque vulnerability assessment and the ability to predict possible future rupture are of vital importance for early diagnosis, prevention and treatment of cardiovascular diseases related to atherosclerosis. It has been hypothesized that critical stress conditions in the plaque may be closely related to plaque rupture and can be combined with current image-based assessment techniques for more accurate plaque evaluation. A major challenge for all available plaque assessment schemes is the lack of gold standard based on in vivo patient data where both ruptured and non-ruptured plaques were compared and analyzed. In vivo patient image data showing rupture verified by histological information (current gold standard) provided by excised specimens data will help to establish in vivo benchmark for image-based and/or stress-based assessment schemes.

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