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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

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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

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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 v

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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

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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 geometri

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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

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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 Atheros

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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

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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

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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

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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 prope

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Books on the topic "Atherosclerotic plague"

1

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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5

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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7

(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"

1

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"

1

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 disru

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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 region

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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 (

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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

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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 principa

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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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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 mechanic

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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

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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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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 pl

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