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Relevant bibliographies by topics / Atherosclerotic plague

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Academic literature on the topic 'Atherosclerotic plague'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Atherosclerotic plague"

1

Zalessky, V. N. "Photodynamic therapy of atherosclerotic plague: the porphyrin sensitizers application." European Journal of Pharmacology 183, no. 4 (1990): 1331. http://dx.doi.org/10.1016/0014-2999(90)94449-8.

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Mubarokah, Siti Nurul, I. Dewa Agung Susilawati, Sumarno Sumarno, I. Ketut Gedhe Muliartha, and Djanggan Sargowo. "Porphyromonas gingivalis Induced Fragmentation of Type IV Collagen Through Macrophage-Activated MMP-9: (In Vitro Study of Collagenolytic Mechanism in Pathogenesis of Atherosclerotic Plaque Rupture)." Indonesian Biomedical Journal 1, no. 3 (2009): 88. http://dx.doi.org/10.18585/inabj.v1i3.105.

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BACKGROUND: Periodontitis is caused mostly by Porphyromonas gingivalis (P.gingivalis) and it is related to acute coronary syndrome. P.gingivalis readily invades blood circulation and potentially induces collagenolytic activity of inflammatory cells that results in collagen vascular degradation leading to atherosclerotic plague rupture (APR). APR is responsible for the occurence of fatal cardiovascular events such as acute myocardial infraction (AMI).AIMS: To show that P.gingivalis potentially induces fragmentation of the type IV vascular collagen due to macrophage-activated MMP-9.MATERIAL AND METHODS: The ability of P.gingivalis to induce the type IV collagen fragmentation, shown by digesting type IV collagen with the supernatant of monocyte-derived macrophage activated by exposure to P.gingivalis suspension for 18 hours, 37oC, 5%CO2. The type IV collagen fragments were analyzed by SDS-PAGE and confirmed by Western-blotting. Antibody of type IV collagen produced and confirmed by dot-blotting prior to its being used as primary antibody of Western-blotting. The existence of MMP-9 was detected by Dot-blot and Western-blot technique, while the MMP-9 activity was assessed by SDS-PAGE and zymograms.RESULTS: Our data showed that P.gingivalis induced macrophage to produce MMP-9 as one of collagenolytic components, and interaction with P.gingivalis proteases enhanced the proteolytic activity and resulted in degradation of type IV collagen with molecular weight of 88 kDa into two smaller fragments with molecular weight of 80 kDa and 60 kDa. CONCLUSION: P.gingivalis induced macrophage to activate its MMP-9 that led to fragmentation of vascular type IV collagen in the pathogenesis of atherosclerotic plaque rupture. KEYWORDS: P.gingivalis, macrophage, type IV collagen fragmentation, atherosclerotic plaque rupture, AMI

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Prabhukumar, Y., and Subhashini . "Knowledge Regarding Prevention of Atherosclerosis Among Young Adults." International Journal of Innovative Science and Research Technology 5, no. 7 (2020): 1354–56. http://dx.doi.org/10.38124/ijisrt20jul827.

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Atherosclerosis is responsible for 50% of all death in Weston societies and it is a chronic inflammatory disease of arteries1 . Heart attacks, stroke and peripheral arterial diseases are developed by atherosclerotic diseases. The incidence is difficult to measure accurately due to its asymptomatic condition. Over 370,000 death occurs annually due to coronary heart disease in the modernized society. Men over 45 years are more predominant to develop plague rupture and it contributes 75% of myocardial infarctions1 . 90% cardiovascular disease related death can be prevented by lifestyle changes. A descriptive study was conducted to evaluate the knowledge of younger adults on prevention of atherosclerosis in outpatient department, Baptist hospital, Bangalore. Hundred voluntaries are enrolled to the study and prior consent was taken. The mean age of the study participant are 29.4 ± 5.2 years and 53.0% were males and 47.0% were females. 34.0% are graduates. In the regards to level of knowledge it was classified as adequate, moderate and Inadequate and the result is 27.0%, 56.0% and 17.0% respectively. The chi-square value of χ 2 = 4.29 (p=0.116) between Educational status and level of knowledge and χ 2 = 4.76 (p=0.092) between gender and level of knowledge shows, there is no statistically significant associations. Pearson correlation coefficient was calculated for age and income with knowledge. The r = 0.08 (p=0.434) of age and knowledge, r = -0.05 (p=0.632) of income and knowledge both shows negligible correlation with no significance.  Conclusion This study concludes that the knowledge on prevention of atherosclerosis among young adults are moderate and there is no relationship was observed with knowledge and educational status, gender, age and income. This result may suggest to have awareness programme on prevention of atherosclerosis among young adults to improve their lifestyle by enhancing the knowledge.

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Millon, Antoine, Emmanuelle Canet-Soulas, Loic Boussel, Zahi Fayad, and Philippe Douek. "Animal models of atherosclerosis and magnetic resonance imaging for monitoring plaque progression." Vascular 22, no. 3 (2014): 221–37. http://dx.doi.org/10.1177/1708538113478758.

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Atherosclerosis, the main cause of heart attack and stroke, is the leading cause of death in most modern countries. Preventing clinical events depends on a better understanding of the mechanism of atherosclerotic plaque destabilization. Our knowledge on the characteristics of vulnerable plaques in humans has grown past decades. Histological studies have provided a precise definition of high-risk lesions and novel imaging methods for human atherosclerotic plaque characterization have made significant progress. However the pathological mechanisms leading from stable lesions to the formation of vulnerable plaques remain uncertain and the related clinical events are unpredictable. An animal model mimicking human plaque destablization is required as well as an in vivo imaging method to assess and monitor atherosclerosis progression. Magnetic resonance imaging (MRI) is increasingly used for in vivo assessment of atherosclerotic plaques in the human carotids. MRI provides well-characterized morphological and functional features of human atherosclerotic plaque which can be also assessed in animal models. This review summarizes the most common species used as animal models for experimental atherosclerosis, the techniques to induce atherosclerosis and to obtain vulnerable plaques, together with the role of MRI for monitoring atherosclerotic plaques in animals.

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Henein, Michael Y., Sergio Vancheri, Gani Bajraktari, and Federico Vancheri. "Coronary Atherosclerosis Imaging." Diagnostics 10, no. 2 (2020): 65. http://dx.doi.org/10.3390/diagnostics10020065.

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Identifying patients at increased risk of coronary artery disease, before the atherosclerotic complications become clinically evident, is the aim of cardiovascular prevention. Imaging techniques provide direct assessment of coronary atherosclerotic burden and pathological characteristics of atherosclerotic lesions which may predict the progression of disease. Atherosclerosis imaging has been traditionally based on the evaluation of coronary luminal narrowing and stenosis. However, the degree of arterial obstruction is a poor predictor of subsequent acute events. More recent techniques focus on the high-resolution visualization of the arterial wall and the coronary plaques. Most acute coronary events are triggered by plaque rupture or erosion. Hence, atherosclerotic plaque imaging has generally focused on the detection of vulnerable plaque prone to rupture. However, atherosclerosis is a dynamic process and the plaque morphology and composition may change over time. Most vulnerable plaques undergo progressive transformation from high-risk to more stable and heavily calcified lesions, while others undergo subclinical rupture and healing. Although extensive plaque calcification is often associated with stable atherosclerosis, the extent of coronary artery calcification strongly correlates with the degree of atherosclerosis and with the rate of future cardiac events. Inflammation has a central role in atherogenesis, from plaque formation to rupture, hence in the development of acute coronary events. Morphologic plaque assessment, both invasive and non-invasive, gives limited information as to the current activity of the atherosclerotic disease. The addition of nuclear imaging, based on radioactive tracers targeted to the inflammatory components of the plaques, provides a highly sensitive assessment of coronary disease activity, thus distinguishing those patients who have stable disease from those with active plaque inflammation.

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Yu, Yan Nan, Ming-Li Li, Yu-Yuan Xu, et al. "Middle cerebral artery geometric features are associated with plaque distribution and stroke." Neurology 91, no. 19 (2018): e1760-e1769. http://dx.doi.org/10.1212/wnl.0000000000006468.

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ObjectiveWe aimed to investigate the geometric features of the middle cerebral artery (MCA) and their relevance to plaque distribution and ischemic stroke.MethodsWe reviewed our institutional vessel wall imaging database. Patients with symptomatic MCA atherosclerosis, asymptomatic MCA atherosclerosis, or without MCA atherosclerosis were included. The MCA geometric features, including M1 segment shape and M1 curve orientation, were defined on magnetic resonance angiography. Plaque distribution and other plaque parameters were identified on vessel wall imaging. The association among MCA geometric features, plaque distribution, and ischemic stroke were analyzed.ResultsA total of 977 MCAs were analyzed (87 atherosclerotic symptomatic MCAs, 459 atherosclerotic asymptomatic MCAs, and 431 plaque-free MCAs). Overall, curved M1 segments were the predominant shape across all groups. In 91.1% of curved atherosclerotic MCAs, the plaque involved the inner wall of the curve. Plaque not involving the inner wall was shorter (p < 0.0001) and thinner (p = 0.005) compared to plaque involving the inner wall. Inferior plaque was observed in 39.9% of inferior-oriented M1 curves compared to 21.7% in non–inferior-oriented M1 curves (p < 0.0001). The absence of an inferior-oriented M1 curve (odds ratio 0.45, 95% confidence interval 0.27–0.77) and presence of superior plaque (odds ratio 2.67, 95% confidence interval 1.52–4.67) were independently associated with stroke after adjusting for plaque length and thickness, degree of stenosis, and remodeling ratio.ConclusionsMCA geometric features are associated with plaque distribution and stroke. Our findings provide insight into the vascular pathophysiology of MCA atherosclerosis.

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Saranchina, J. V., S. V. Dutova, O. Y. Kilina, N. V. Khanarin, and T. S. Kulakova. "Features of interleukin-19 production in patients with atherosclerosis." Siberian Journal of Clinical and Experimental Medicine 36, no. 2 (2021): 52–60. http://dx.doi.org/10.29001/2073-8552-2021-36-2-52-60.

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Objective. To study the features of local and systemic production of interleukin-19 in patients with atherosclerosis.Material and Methods. The study comprised a total of 46 patients (26 women and 20 men) treated for arterial hypertension in the therapeutic department of Republican Clinical Hospital named after G.Y. Remishevskaya. The mean age of subjects was 63.4 ± 3.2 years. The control group included 40 patients (23 women and 17 men aged 44.7 ± 5.5 years) who did not have atherosclerosis. Samples of atherosclerotic plaques and venous blood were examined. Atherosclerotic plaques were obtained by endarterectomy and then subjected to homogenization followed by enzymatic hydrolysis for 1 h at 37 °C with collagenase IV in the presence of proteinase III inhibitors. The serum levels of cytokines (in the control group and in patients with atherosclerosis) and in the atherosclerotic plaque homogenate (in patients with atherosclerosis) were determined by ELISA. To assess the cytokine-producing capacity of blood leukocytes and white blood cells isolated from atherosclerotic plaques, spontaneous and phytohemagglutinin (PHA)-induced cytokine production was determined when the cells were cultured in RPMI-1640.Results. The serum levels of IL-19 did not significantly differ between the patients with atherosclerosis and the control group. A statistically significant two-fold increase in the spontaneous expression of IL-19 by blood leukocytes was observed in the group of patients with atherosclerosis in comparison with the control group. When comparing the contents of IL-19 in blood serum and atherosclerotic plaque homogenate in patients with atherosclerosis, no statistically significant differences were found (p = 0.182). The level of PHA-induced IL-19 production by the atherosclerotic plaque white blood cells was significantly lower than that of blood leucocytes.Conclusion. The study showed that the reserve capacity for IL-19 synthesis in the atherosclerotic plaque white blood cells decreases leading to the progression of inflammation. The obtained results suggest that IL-19 plays the anti-atherogenic role and its production is involved in the maintaining the mechanisms for down-regulation of inflammation in atherosclerotic plaques.

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Hartman, Robin J. G., Katie Owsiany, Lijiang Ma, et al. "Sex-Stratified Gene Regulatory Networks Reveal Female Key Driver Genes of Atherosclerosis Involved in Smooth Muscle Cell Phenotype Switching." Circulation 143, no. 7 (2021): 713–26. http://dx.doi.org/10.1161/circulationaha.120.051231.

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Background: Although sex differences in coronary artery disease are widely accepted with women developing more stable atherosclerosis than men, the underlying pathobiology of such differences remains largely unknown. In coronary artery disease, recent integrative systems biological studies have inferred gene regulatory networks (GRNs). Within these GRNs, key driver genes have shown great promise but have thus far been unidentified in women. Methods: We generated sex-specific GRNs of the atherosclerotic arterial wall in 160 women and age-matched men in the STARNET study (Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task). We integrated the female GRNs with single-cell RNA-sequencing data of the human atherosclerotic plaque and single-cell RNA sequencing of advanced atherosclerotic lesions from wild type and Klf4 knockout atherosclerotic smooth muscle cell (SMC) lineage-tracing mice. Results: By comparing sex-specific GRNs, we observed clear sex differences in network activity within the atherosclerotic tissues. Genes more active in women were associated with mesenchymal cells and endothelial cells, whereas genes more active in men were associated with the immune system. We determined that key drivers of GRNs active in female coronary artery disease were predominantly found in (SMCs by single-cell sequencing of the human atherosclerotic plaques, and higher expressed in female plaque SMCs, as well. To study the functions of these female SMC key drivers in atherosclerosis, we examined single-cell RNA sequencing of advanced atherosclerotic lesions from wild type and Klf4 knockout atherosclerotic SMC lineage-tracing mice. The female key drivers were found to be expressed by phenotypically modulated SMCs and affected by Klf4, suggesting that sex differences in atherosclerosis involve phenotypic switching of plaque SMCs. Conclusions: Our systems approach provides novel insights into molecular mechanisms that underlie sex differences in atherosclerosis. To discover sex-specific therapeutic targets for atherosclerosis, an increased emphasis on sex-stratified approaches in the analysis of multi-omics data sets is warranted.

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Carresi, Cristina, Rocco Mollace, Roberta Macrì, et al. "Oxidative Stress Triggers Defective Autophagy in Endothelial Cells: Role in Atherothrombosis Development." Antioxidants 10, no. 3 (2021): 387. http://dx.doi.org/10.3390/antiox10030387.

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Atherothrombosis, a multifactorial and multistep artery disorder, represents one of the main causes of morbidity and mortality worldwide. The development and progression of atherothrombosis is closely associated with age, gender and a complex relationship between unhealthy lifestyle habits and several genetic risk factors. The imbalance between oxidative stress and antioxidant defenses is the main biological event leading to the development of a pro-oxidant phenotype, triggering cellular and molecular mechanisms associated with the atherothrombotic process. The pathogenesis of atherosclerosis and its late thrombotic complications involve multiple cellular events such as inflammation, endothelial dysfunction, proliferation of vascular smooth muscle cells (SMCs), extracellular matrix (ECM) alterations, and platelet activation, contributing to chronic pathological remodeling of the vascular wall, atheromatous plague formation, vascular stenosis, and eventually, thrombus growth and propagation. Emerging studies suggest that clotting activation and endothelial cell (EC) dysfunction play key roles in the pathogenesis of atherothrombosis. Furthermore, a growing body of evidence indicates that defective autophagy is closely linked to the overproduction of reactive oxygen species (ROS) which, in turn, are involved in the development and progression of atherosclerotic disease. This topic represents a large field of study aimed at identifying new potential therapeutic targets. In this review, we focus on the major role played by the autophagic pathway induced by oxidative stress in the modulation of EC dysfunction as a background to understand its potential role in the development of atherothrombosis.

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Worthmann, Anna, Christian Schlein, Jimmy Berbée, Patrick Rensen, Joerg Heeren, and Alexander Bartelt. "Effects of Pharmacological Thermogenic Adipocyte Activation on Metabolism and Atherosclerotic Plaque Regression." Nutrients 11, no. 2 (2019): 463. http://dx.doi.org/10.3390/nu11020463.

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Thermogenic adipocytes burn nutrients in order to produce heat. Upon activation, brown adipose tissue (BAT) clears vast amounts of lipids and glucose from the circulation and thus substantially lowers plasma lipid levels. As a consequence, BAT activation protects from the development of atherosclerosis. However, it is unclear if pharmacologic activation of BAT can be exploited therapeutically to reduce plaque burden in established atherosclerotic disease. Here we study the impact of thermogenic adipose tissues on plaque regression in a mouse model of atherosclerosis. Thermogenic adipocytes in atherosclerotic low-density lipoprotein (LDL) receptor (LDLR)-deficient mice were pharmacologically activated by dietary CL316,243 (CL) treatment for 4 weeks and the outcomes on metabolically active tissues, plasma lipids and atherosclerosis were analyzed. While the chronic activation of thermogenic adipocytes reduced adiposity, increased browning of white adipose tissue (WAT), altered liver gene expression, and reduced plasma triglyceride levels, atherosclerotic plaque burden remained unchanged. Our findings suggest that despite improving adiposity and plasma triglycerides, pharmacologic activation of thermogenic adipocytes is not able to reverse atherosclerosis in LDLR-deficient mice.

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Dissertations / Theses on the topic "Atherosclerotic plague"

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Shakya, Arvind. "Mechanism of matrix metalloproteinase-14 (mmp-14) regulation during atherosclerosis." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4436.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.<br>"December 2006" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

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McCord, Barbara Norton. "Fatigue of atherosclerotic plaque." Diss., Georgia Institute of Technology, 1992. http://hdl.handle.net/1853/15890.

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Zhu, Chengcheng. "High resolution black blood magnetic resonance imaging of atherosclerotic plaque." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648792.

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Obaid, Daniel Rhys. "Coronary atherosclerotic plaque imaging." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608243.

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Lilledahl, Magnus Borstad. "Detection of Vulnerable Atherosclerotic Plaque." Doctoral thesis, Norwegian University of Science and Technology, Department of Electronics and Telecommunications, 2007. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1506.

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<p>Heart attacks are the cause for the majority of deaths in the industrialized world. The underlying cause of most of these deaths is the rupture of vulnerable plaque. As of this day, no widely accepted clinical tool exists for detecting plaques that are prone to rupture, although several techniques are being investigated. This thesis gives an overview of detection modalities that have been proposed for detecting vulnerable plaque with special emphasis on three methods, diffuse reflection spectroscopy, thermography and multiphoton microscopy.</p>

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Calvert, Patrick Andrew. "Virtual-histology intravascular ultrasound in vulnerable atherosclerosis." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609857.

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Loree, Howard Martin. "The mechanics of atherosclerotic plaque rupture." Thesis, Massachusetts Institute of Technology, 1992. http://hdl.handle.net/1721.1/17301.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Whitaker College of Health Sciences and Technology, 1992.<br>Includes bibliographical references (leaves 139-146).<br>by Howard M. Loree II.<br>Ph.D.

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Kim, Taehong. "Thermal study of vulnerable atherosclerotic plaque." [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-2541.

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Lee, Regent. "Biomarkers of coronary atherosclerotic plaque rupture." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:7f0136bf-ad55-4dc8-bcc3-1d55cb269ef8.

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Coronary atherosclerotic plaque rupture is a critical event during atherosclerosis disease progression. Clinical consequences of atherosclerotic plaque rupture vary from asymptomatic to acute arterial thrombosis, yet the mechanisms underpinning such divergent biological response remain poorly understood. Novel biological signatures of plaque rupture will confer further insights into the dynamic responses triggered by plaque rupture event(s), and may provide alternative strategies for modulation of this prevalent disease. This thesis aims to investigate the events that accompany coronary plaque rupture and their relations to subsequent, downstream systemic effects. In a prospective clinical study of patients undergoing non-emergency percutaneous coronary intervention (PCI), stenting induced plaque disruption was used as a model of plaque rupture in vivo. Optical coherence tomography (OCT) imaging of the plaque lesion was performed prior to stenting, followed by serial blood sampling from targeted anatomical sites in reference to the plaque disruption event. Coronary plaque debris were also retrieved in a controlled manner. Analysis of candidate markers demonstrated a role of matrix metalloproteinase 9 (MMP9) in the systemic response to plaque disruption. Local and systemic elevations of MMP9 were observed promptly after plaque disruption. The systemic release of MMP9 was independent to the myocardial injury and systemic inflammation as a result of PCI. OCT analysis further suggested that plaque morphology may be a determining factor in the subsequent MMP9 release, as the disruption of lipid rich plaque(s) resulted in more acute elevation 'of ~1'MP9 when compared to disruption of non-lipid lesions. Changes of systemic MMP9 served as an index of response to the stent induced plaque disruption. Subjects with divergent MMP9 responses to the plaque disruption event were put forward for further comprehensive investigation during the discovery phase, using mass spectrometry techniques to investigate the lipidomic, metabolomics, and proteomic signatures of plaque disruption. Coronary atherosclerotic plaque disruption was associated with immediate changes in the plasma lipidomics and metabolomics profiles, which had distinct relations to the subsequent systemic MMP9 release. Coronary plaque debris provided a "catalogue" of proteins which could be acutely liberated into systemic circulation. Several such novel proteins were detected in circulation after plaque disruption, which triggered disparate responses in known canonical pathways. Evidence from this thesis implicates the role of liver X receptor / retinoic acid receptor pathway (LXR/RXR) as a key mediator to the divergent systemic responses after plaque disruption, and pinpoints a direction for future investigations.

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Sun, Binjian. "Multicontrast MRI of Atherosclerotic Plaques: Acquisition, Characterization and Reconstruction." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/16291.

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Cardiovascular Disease (CVD) continues to be the leading cause of death in western countries according to the statistics update by the American Heart Association. Atherosclerosis is estimated to be responsible for a large portion of CVD and affects 60 million people in the United States. Accurate diagnosis is crucial for proper treatment planning. Currently, the clinical standard screening technique for diagnosing atherosclerosis is x-ray angiography, which reveals the residual lumen size. X-ray angiographic images possess good resolution and contrast, however, lumen size is not always a proper criterion given the positive remodeling nature of atherosclerotic plaques. In the past decade, it has been shown that most plaques responsible for a fatal or nonfatal myocardial infarction are less than 70% stenosed. Clinical data support the idea that plaques producing non-flow-limiting stenoses account for more cases of plaque rupture and thrombosis than plaques producing a more severe stenosis. Due to this fact, plaque itself must be imaged in order to assess its vulnerability. A wealth of literature suggests that multicontrast MRI has the potential of characterizing plaque constituents, and thus is a promising technique for plaque imaging. Because of the technical difficulties associated with in-vivo plaque imaging and the fact that our research was aimed at developing new methodologies, our approaches was to image excised coronary arteries under simulated in-vivo conditions in a tissue culture chamber. It is shown by this research that automatic plaque characterization techniques developed under ex-vivo conditions still apply for in-vivo studies. Based on this finding, an automatic plaque characterization technique using multicontrast MRI was developed. Furthermore, "shared k-space" reconstruction techniques were interrogated to assess their feasibility in accelerating multicontrast MRI acquisition. Results show that these techniques are promising in accelerating multicontrast MRI acquisitions.

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Books on the topic "Atherosclerotic plague"

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George, Sarah J., and Johnson Jason. Atherosclerosis: Molecular and cellular mechanisms. Wiley-VCH, 2010.

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Virmani, Renu, Jagat Narula, Martin B. Leon, and James T. Willerson, eds. The Vulnerable Atherosclerotic Plaque. Blackwell Publishing, 2006. http://dx.doi.org/10.1002/9780470987575.

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Glagov, Seymour, William P. Newman, and Sheldon A. Schaffer, eds. Pathobiology of the Human Atherosclerotic Plaque. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3326-8.

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NATO Advanced Research Workshop on Progress, Problems, and Promises for an Effective Quantitative Evaluation of Atherosclerosis in Living and Autopsied Experimental Animals and Man (1990 Siena, Italy). Atherosclerotic plaques: Advances in imaging for sequential quantitative evaluation. Edited by Wissler Robert W. 1917- and North Atlantic Treaty Organization. Scientific Affairs Division. Plenum Press, 1991.

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Sinatra, Stephen T. Reverse heart disease now: Stop deadly cardiovascular plaque before it's too late. John Wiley & Sons, 2007.

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C, Merrell Woodson, and Thornton James 1952-, eds. The arginine solution: The first guide to America's new cardio-enhancing supplement. Warner Books, 1999.

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(Editor), Ron Waksman, Patrick W. Serruys (Editor), and Johannes Schaar (Editor), eds. The Vulnerable Plaque, Second Edition. 2nd ed. Informa Healthcare, 2007.

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Ramrakha, Punit, and Jonathan Hill, eds. Coronary artery disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0005.

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Atherosclerosis: pathophysiology 212Development of atherosclerotic plaques 214Epidemiology 216Assessment of atherosclerotic risk 218Risk factors for coronary artery disease 220Hypertension 226Treatment of high blood pressure 228Combining antihypertensive drugs 230Lipid management in atherosclerosis 232Lipid-lowering therapy 236When to treat lipids ...

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Fuster, Valentin, and William Insull. Assessing and Modifying the Vulnerable Atherosclerotic Plaque. Wiley & Sons, Incorporated, John, 2008.

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Valentin, Fuster, and Insull William, eds. Assessing and modifying the vulnerable atherosclerotic plaque. Futura Pub. Co., 2002.

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Book chapters on the topic "Atherosclerotic plague"

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Abrams, David B., J. Rick Turner, Linda C. Baumann, et al. "Atherosclerotic Plaque." In Encyclopedia of Behavioral Medicine. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100126.

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Lavin Plaza, Begoña, Pierre Gebhardt, Alkystis Phinikaridou, and René M. Botnar. "Atherosclerotic Plaque Imaging." In Protocols and Methodologies in Basic Science and Clinical Cardiac MRI. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53001-7_8.

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Piro, Maddalena, Sara di Michele, and Massimo Fioranelli. "The Atherosclerotic Plaque." In CT Evaluation of Coronary Artery Disease. Springer Milan, 2009. http://dx.doi.org/10.1007/978-88-470-1126-7_6.

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Lavin-Plaza, Begoña, Alkystis Phinikaridou, Marcelo E. Andia, et al. "Atherosclerotic Plaque Imaging." In Contemporary Cardiology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8841-9_14.

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Gooch, Jan W. "Atherosclerotic Plaques." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13185.

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Vinduška, V., I. Dittert, V. Horáček, et al. "Photosensitization of Atherosclerotic Plaque." In Laser in der Medizin / Laser in Medicine. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-93548-0_35.

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Schoenhagen, Paul, Anuja Nair, Stephen Nicholls, and Geoffrey Vince. "Assessment of Plaque Burden and Plaque Composition Using Intravascular Ultrasound." In Asymptomatic Atherosclerosis. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-179-0_36.

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Khaw, Ban-An. "Targeting Atherosclerotic Plaques." In Biomedical Aspects of Drug Targeting. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-4627-3_4.

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Kyriacou, Efthyvoulos, Christodoulos I. Christodoulou, Marios S. Pattichis, Constantinos S. Pattichis, and Stavros K. Kakkos. "Plaque Classification." In Ultrasound and Carotid Bifurcation Atherosclerosis. Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-688-5_15.

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Bonnet, J., and D. Benchimol. "How does the Clinician Evaluate the Atherosclerotic Plaque Quantitatively?" In Atherosclerotic Plaques. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-0438-9_6.

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Conference papers on the topic "Atherosclerotic plague"

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Campbell, Ian C., Daiana Weiss, John N. Oshinski, and W. Robert Taylor. "Histological Determination of Murine Plaque Mechanics and Implications for Plaque Rupture." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19295.

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Among the most common models in atherosclerosis research is the atherosclerosis-prone mouse. Genetically manipulated mouse strains such as the ApoE−/− mouse will reliably form plaques under certain conditions, and these lesions have been noted to exhibit morphological and biochemical similarities with human atherosclerotic plaques. Unlike plaques in humans, however, murine plaques are not observed to rupture and form occlusive thrombi [1]. As atherosclerosis and its complications are the leading cause of death in the modern world, a comprehensive understanding of the mechanisms of plaque disruption is essential to develop diagnostic and interventional techniques. Although the mouse model is frequently employed to study plaque formation, its validity for studying plaque disruption events such as rupture or erosion has been questioned.

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Liu, Biyue, and Dalin Tang. "Computer Simulations of the Blood Flows and the Growth of Stenosis in Arteries With Bends and Bifurcations." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203654.

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Heart attack and stroke are the chief and the 3rd largest causes of death in the United States, respectively. A heart attack occurs when the blood supply to an area of heart muscle is blocked, usually by a clot in a coronary artery; a stroke occurs when the blood supply to a region of the brain is lost. The most frequent cause of loss of blood supply to brain tissue or to heart muscle is atherosclerosis, which involves complex interactions between the artery wall and the blood flow. Caro et al first suggested that the distribution of fatty streaking in human aorta may be coincident with regions in which the shear rate at the arterial wall is locally reduced [1]. After that, intensive research has been conducted to statistically study the role of shear stress in atherosclerosis and to quantitatively determine the correlation between the low shear stress and the development of atherosclerotic plaques [2–8]. It is widely believed that fluid shear stress acting on the artery wall plays an important role in the pathogenesis of atherosclerosis. The objectives of this project are to investigate how the geometrical adaptation of atherosclerotic plaques is related to the wall shear stress (WSS) and to study the influences of the flow parameters on the growth of the atherosclerotic plaque using computational models.

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Gijsen, Frank, Hans Schuurbiers, Michiel Schaap, Anton van der Steen, and Jolanda Wentzel. "A New 3D Reconstruction Method for Human Coronary Bifurcations for Shear Stress Computations." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80251.

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Atherosclerosis is characterized by lipid accumulation in the arterial wall, followed by an inflammatory response. Plaque formation is generally observed near bifurcations in coronary arteries. The composition of atherosclerotic plaques depends on the location, and it was hypothesized that blood flow induced shear stress influences plaque composition2. To study the impact of shear stress on atherosclerotic disease in human coronary arteries, we developed a technique that enables us to generate 3D lumen reconstruction based on multislice computer tomography (MSCT) and intravascular ultrasound (IVUS).We describe two approaches to generate 3D reconstructions of human coronary artery bifurcations and apply them to coronary segments with bifurcations. We will evaluate the effect on shear stress distribution and its relationship to wall thickness.

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Van der Heiden, K., H. C. Groen, P. C. Evans, et al. "Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80515.

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Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.

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Mondal, Sayan, Chun Yang, Joseph D. Petruccelli, et al. "A New Hypothesis for Human Atherosclerotic Plaque Progression Based on Serial In Vivo MRI and Computational Modeling Method." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175504.

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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].

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Akyildiz, A. C., L. Speelman, H. Nieuwstadt, et al. "The Effect of Plaque Morphology on Cap Stresses in Coronary Arteries." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80647.

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Atherosclerosis is a cardiovascular disease characterized by plaque formation in the vessel wall. The region of an atherosclerotic plaque separating its pathological content from the lumen is called cap. Cap rupture initiates thrombus formation and may lead to myocardial infarction and sudden death [1].

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7

Teng, Zhongzhao, Allen H. Hoffman, Jie Zheng, Pamela K. Woodard, and Dalin Tang. "Ultimate Strength of the Adventitia and Media of Human Atherosclerotic Carotid Arteries in the Axial and Circumferential Directions." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204715.

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The abrupt closure of an artery by an occlusive thrombus is the main cause of myocardial infarcts and other thrombotic sequelae of atherosclerosis. This thrombosis is often associated with rupture of an atherosclerotic plaque [1,2]. Histology has shown that most rupture sites are also sites of increased mechanical stress [2]. It has been widely accepted that atherosclerosis leads to locally increased stresses in the region of lesions. However, validation of this hypothesis has been impeded by a lack of experimental data on the material strength of atherosclerotic tissues. Knowledge of mechanical properties of human atherosclerotic tissues is essential for understanding the rupture mechanism and also for creating more accurate computational models for predicting fatal cardiovascular events [3]. Moreover, an increased understanding of the mechanical properties of atherosclerotic tissue is important for developing greater insight into the pathophysiology of the cardiovascular system and as well as for predicting the outcome of interventional treatments such as balloon angioplasty.

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8

Sarker, Sunandita, Yiannis S. Chatzizisis, Srivatsan Kidambi, and Benjamin S. Terry. "Design and Development of a Novel Drug Delivery Catheter for Atherosclerosis." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6869.

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Atherosclerosis is a chronic progressive cardiovascular disease that results from plaque formation in the arteries. It is one of the leading causes of death and loss of healthy life in modern world. Atherosclerosis lesions consist of sub-endothelial accumulations of cholesterol and inflammatory cells [1]. However, not all lesions progress to the final stage to cause catastrophic ischemic cardiovascular events [2]. Early identification and treatment of high-risk plaques before they rupture, and precipitate adverse events constitutes a major challenge in cardiology today. Numerous investigations have confirmed that atherosclerosis is an inflammatory disease [3] [4] [5]. This confirmation has opened the treatment of this disease to many novel anti-inflammatory therapeutics. The use of nanoparticle-nanomedicines has gained popularity over recent years. Initially approved as anticancer treatment therapeutics [6], nanomedicine also holds promise for anti-inflammatory treatment, personalized medicine, target-specific treatment, and imaging of atherosclerotic disease [7]. The primary aim of this collaborative work is to develop and validate a novel strategy for catheter-directed local treatment of high-risk plaque using anti-inflammatory nanoparticles. Preselected drugs with the highest anti-inflammatory efficacy will be incorporated into a novel liposome nanocarrier, and delivered in-vivo through a specially designed catheter to high-risk atherosclerotic plaques. The catheter has specially designed perfusion pores that inject drug into the blood stream in such a controlled manner that the streamlines carry the nanoparticles to the stenotic arterial wall. Once the particles make it to the arterial wall, they can be absorbed into the inflamed tissue. In this paper, we discuss the design and development of an atraumatic drug delivery catheter for the administration of lipid nanoparticles.

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9

van der Heiden, Kim, Harald C. Groen, Lambert Speelman, et al. "Correlation Between Plaque Composition and Shear Stress Using Three-Dimensional Reconstructed Histology and Computational Fluid Dynamics of Diseased Human Carotid Arteries." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53639.

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Wall shear stress (WSS) has been shown to play a crucial role in atherosclerotic plaque formation and progression. Moreover, some recent studies suggest that WSS is also involved in determining plaque composition (Cheng et al., 2006) and plaque destabilization in advanced atherosclerosis (Groen et al., 2007). More detailed studies on the relationship between WSS and plaque composition are needed to confirm those relationships.

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10

Teng, Zhongzhao, Joseph D. Petruccelli, Xueying Huang, et al. "Atherosclerotic Carotid Plaques With Prior Rupture Are Associated With Higher Structural Stresses: In Vivo MRI-Based 3D FSI Studies." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204708.

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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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