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34 - Molecular imaging of carotid artery disease
- from Future directions in carotid plaque imaging
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- By James H. F. Rudd, The Zena and Michael A. Wiener Cardiovascular Institute, The Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York NY, USA, Michael J. Lipinski, The Zena and Michael A. Wiener Cardiovascular Institute, The Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York NY, USA, Fabien Hyafil, The Zena and Michael A. Wiener Cardiovascular Institute, The Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York NY, USA, Zahi A. Fayad, The Zena and Michael A. Wiener Cardiovascular Institute, The Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York NY, USA
- Edited by Jonathan Gillard, University of Cambridge, Martin Graves, University of Cambridge, Thomas Hatsukami, University of Washington, Chun Yuan, University of Washington
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- Book:
- Carotid Disease
- Published online:
- 03 December 2009
- Print publication:
- 07 December 2006, pp 471-483
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- Chapter
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Summary
Atherosclerosis and its complications are the scourge of Western civilization, and are becoming increasingly more frequent in the developing world (British Heart Foundation Health Promotion Research Group, 2005). Atherosclerosis affects medium- and large-sized arteries, with the carotid artery being the second most common site after the thoracic aorta (Svindland and Torvik, 1988).
Atherosclerosis is characterized by accumulation of lipid, inflammatory cells and connective tissue within the arterial wall. It is a chronic, progressive disease that has a long asymptomatic phase. The first pathological abnormality is the fatty streak, caused by an aggregation of lipid and macrophages in the subendothelial space. The fatty streak, often present within the aorta from the second decade of life (Ross, 1999), is thought to develop primarily in regions of endothelial dysfunction. Endothelial cells in regions of disrupted flow and low shear stress, often occurring in branch or bifurcation points of the arterial tree (Vander Laan et al., 2004), have decreased production of nitric oxide (Ku et al., 1985). The low shear stress also leads to increased expression of adhesion molecules and uptake of lipoproteins into the subendothelial space by means still unclear (Kinlay et al., 1998). Once oxidized, low density lipoproteins (LDL) are retained in the subendothelial space. Oxidized LDL (oxLDL) contains monocyte chemoattractant factors such as lysophosphatidylcholine and attracts further monocytes by triggering the release of monocyte chemoattractant protein-1 (MCP-1) from endothelial cells and smooth muscle cells (Cushing et al., 1990).
13 - Atherosclerosis
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- By James H. F. Rudd, Peter L. Weissberg, School of Clinical Medicine, University of Cambridge, Cambridge
- Edited by Beverley J. Hunt, University of London, Lucilla Poston, University of London, Michael Schachter, Imperial College of Science, Technology and Medicine, London, Alison W. Halliday, St George's Hospital, London
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- Book:
- An Introduction to Vascular Biology
- Published online:
- 07 September 2009
- Print publication:
- 25 July 2002, pp 302-317
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Summary
Introduction
Atherosclerosis continues to be a leading cause of mortality and morbidity throughout the world. It has until recently been thought of as a degenerative disease, affecting predominantly older people, with progression over several decades, and eventually leading to symptoms through its mechanical effects on blood flow, particularly in the small-calibre arteries supplying the myocardium and brain. Because of the perceived insidious and relentless nature of its development, there has been a somewhat pessimistic view of the potential to modify its progression by medical therapy, and treatment has instead been dominated by interventional revascularization approaches, targeting the largest and most visible or symptomatic lesions with angioplasty or bypass surgery. There has been little emphasis on the diagnosis and quantification of subclinical disease, or the treatment of high-risk, asymptomatic patients. Recently, this defeatist view of the pathogenesis and progression of atherosclerosis has begun to change, firstly, because careful descriptive studies of the underlying pathology of atherosclerosis have revealed that atherosclerotic plaques differ in their cellular composition, and that the cell types predominating in the plaque can determine the risk of a fatal clinical event such as myocardial infarction or stroke. Secondly, cellular and molecular biological studies, particularly involving transgenic mice, have emphasized the importance of inflammatory cells and inflammatory mediators in the pathogenesis of atherosclerosis.