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Published: 9 March 2023
Last updated: 10 March 2023

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1

Taylor, Allen J., and Todd C. Villines, eds. Atherosclerosis: Clinical Perspectives Through Imaging. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4288-1.

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2

G, Olsson Anders, and European Atherosclerosis Society, eds. Atherosclerosis: Biology and clinical science. Edinburgh: Churchill Livingstone, 1987.

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3

Boris, Draznin, and Eckel Robert H, eds. Diabetes and atherosclerosis: Molecular basis and clinical aspects. New York: Elsevier, 1993.

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4

Heparin and the prevention of atherosclerosis: Basic research and clinical application. New York: Wiley-Liss, 1990.

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5

Arnold O. Beckman Conference in Clinical Chemistry. (11th 1988 Phoenix, Ariz.). Atherosclerosis: Metabolism, risk, and control : the Eleventh Annual Arnold O. Beckman Conference in Clinical Chemistry, January 18-20, 1988, Phoenix, Arizona. [Chicago, Ill.]: American Association for Clinical Chemistry, 1988.

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6

1928-, Strandness D. E., ed. Vascular diseases: Current research and clinical applications. Orlando: Grune & Stratton, 1987.

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7

Eckardstein, Arnold von. High Density Lipoproteins: From Biological Understanding to Clinical Exploitation. Cham: Springer Nature, 2015.

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8

1956-, Davidson Michael, and International Conference on Atherosclerosis (2000 : Stockholm, Sweden), eds. A symposium: Utilization of surrogate markers of atherosclerosis for the clinical development of pharmaceutical agents. New York: Excerpta Medica, 2001.

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9

W, Liepsch D., ed. Blood flow in large arteries: Applications to atherogenesis and clinical medicine. Basel: Karger, 1990.

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10

Bergstrand, Lott. Femoral and coronary atherosclerosis in patients with hyperlipidaemia: Arteriographic findings correlated to clinical and biochemical parameters. Copenhagen: Munksgaard, 1994.

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11

C, Diehm, Sinzinger H, and Rogatti W. 1947-, eds. Prostaglandin E₁: New aspects on pharmacology, metabolism, and clinical efficacy. Berlin: Springer-Verlag, 1991.

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12

Olsson, G. Anders. Atherosclerosis: Biology and Clinical Science. Churchill Livingstone, 1987.

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13

Atherosclerosis Clinical Perspectives Through Imaging. Springer, 2013.

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14

Taylor, Allen J., and Todd C. Villines. Atherosclerosis: Clinical Perspectives Through Imaging. Springer, 2016.

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15

Villines, Todd C., and Allen J. Taylor. Atherosclerosis: Clinical Perspectives Through Imaging. Springer London, Limited, 2012.

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16

Land, Stephen C., Yves Audigier, Michiko Watanabe, and Carla Costa. Clinical Assessment and Treatment Atherosclerosis. DI Press, 2022.

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17

Manning, G. Atherosclerosis: Metabolic, Morphologic, and Clinical Aspects. Springer, 2012.

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18

Manning, G. Atherosclerosis: Metabolic, Morphologic, and Clinical Aspects. Springer London, Limited, 2013.

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19

Leira, Enrique C. Unusual Causes of Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0105.

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Unusual causes of stroke include those etiologies of cerebral infarction that are not related to the most common mechanisms of atherosclerosis or cardioembolism. This category includes non-atherosclerotic arteriopathies such as arterial dissection, moyamoya, and central nervous system (CNS) vasculitis. It also includes strokes related to a hypercoagulable state. Because the prevalence of atherosclerosis increases with age, unusual causes of stroke are more commonly seen in younger individuals in whom stroke is often not suspected, and therefore not readily diagnosed. Due to the relative rarity, these patients are difficult to test in clinical trials, which makes progress in management challenging.
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20

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.
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21

Stokes, Joseph. Hypercholesterolemia: Clinical and Therapeutic Implications (Atherosclerosis Reviews). Raven Pr, 1988.

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22

Bond, M. Gene. Clinical Diagnosis of Atherosclerosis: Quantitative Methods of Evaluation. Springer, 2012.

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23

Drew, Angela F. Atherosclerosis: Experimental Methods and Protocols. Humana Press, 2010.

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24

Atherothrombosis in Clinical Practice. Oxford University Press, Incorporated, 2013.

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25

Atherothrombosis in Clinical Practice. Oxford University Press, Incorporated, 2013.

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26

Atherothrombosis in Clinical Practice. Oxford University Press, 2013.

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27

Draznin, Boris. Diabetes and Atherosclerosis: Molecular Basis and Clinical Aspects. Oxford University Press, 1993.

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28

Bond, M. Gene. Clinical Diagnosis of Atherosclerosis: Quantitative Methods of Evaluation. Springer London, Limited, 2012.

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29

Syndromes of atherosclerosis: Correlations of clinical imaging and pathology. Armonk, NY: Futura Pub. Co., 1996.

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30

Catapano, Alberico L., and Franco Bernini. High Density Lipoproteins: Physiopathology and Clinical Relevance (Atherosclerosis Reviews). Raven Pr, 1993.

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31

(Editor), Valentin Fuster, Herbert C. Stary (Editor), a. Bleakley Chandler (Editor), Seymour Glagov (Editor), William Insull (Editor), Michael E. Rosenfeld (Editor), Colin J. Schwartz (Editor), William D. Wagner (Editor), and Robert D. Wissler (Editor), eds. Syndromes of Atherosclerosis: Correlations of Clinical Imaging and Pathology. Futura Publishing Company, 1996.

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32

Biochemistry of Atherosclerosis (Advances in Biochemistry in Health and Disease Book 1). Springer, 2006.

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33

Wentzel, Jolanda J., Ethan M. Rowland, Peter D. Weinberg, and Robert Krams. Biomechanical theories of atherosclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0012.

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Atherosclerosis, the disease underlying most heart attacks and strokes, occurs predominantly at certain well-defined sites within the arterial system. Its development may therefore depend not only on systemic risk factors but also on locally varying biomechanical forces. There are three inter-related theories explaining the effect of biomechanics on atherosclerosis. In the first theory, a central role is played by lipid transport into the vessel wall, which varies as a result of mechanical forces. In the second theory, haemodynamic wall shear stress-the frictional force per unit area of endothelium arising from the movement of blood-activates signalling pathways that affect endothelial cell properties. In the third, strain-the stretch of the wall arising from changes in blood pressure-is the key biomechanical trigger. All three theories are discussed from historical, molecular, and clinical perspectives.
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34

Catapano, Alberico L., and Gianfranco Salvioli. High-Density Lipoproteins: Physiopathological Aspects and Clinical Significance (Atherosclerosis Reviews). Raven Pr, 1987.

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35

Biochemistry of Atherosclerosis (Advances in Biochemistry in Health and Disease). Springer, 2006.

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36

Atherosclerosis: Experimental Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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37

Cannon, Richard O. Endothelium, Nitric Oxide, and Atherosclerosis: From Basic Mechanisms to Clinical Implications. Blackwell Publishing Limited, 1999.

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38

Brown, David. Cardiovascular Plaque Rupture (Fundamental and Clinical Cardiology, 45). Informa Healthcare, 2002.

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39

Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
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40

Nixdorff, Uwe, Stephan Achenbach, Frank Bengel, Pompillio Faggiano, Sara Fernández, Christian Heiss, Thomas Mengden, et al. Imaging in cardiovascular prevention. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0006.

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Imaging tools in preventive cardiology can be divided into imaging modalities to assess pre-clinical and clinical atherosclerosis and functional assessments of vascular function or vascular inflammation. To calculate the likelihood of pre-clinical atherosclerosis intima-media thickness as well as coronary calcium scoring are most frequently used. However, beyond these two there are other parameters derived by ultrasound and multi-detector computed tomography as well as magnetic resonance imaging and nuclear/molecular imaging which are discussed in the chapter. Functional tests include flow-mediated dilatation, pulse wave analysis, and the ankle-brachial index. In clinical research other invasive measurements such as intravascular ultrasound/virtual histology/elastography, optical coherence tomography as well as thermography are being used. However, their value in clinical prevention still needs to be established.
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41

Liepsch, D. W. Blood Flow in Large Arteries: Applications to Atherogenesis and Clinical Medicine (Monographs on Atherosclerosis). S. Karger Publishers (USA), 1990.

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42

Holdt, Lesca M., and Daniel Teupser. Genetic background of atherosclerosis and its risk factors. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0002.

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This chapter is concerned with how atherosclerosis risk is modulated by a complex interplay between genetic and environmental risk factors. The contribution of genetics to the variability of atherosclerosis risk is estimated as 50%. Recent genome-wide association studies have led to the identification of over 50 gene variants which modulate atherogenesis. Risk factors for atherosclerosis are also partly genetically determined and some of the variants which play a role in atherogenesis overlap with those modulating its risk factors. However, the current relevance of these findings for clinical practice is limited, mainly due to the small effect sizes of identified risk variants with insufficient discriminatory power, and a large portion of the genetic contribution to atherosclerosis is still unknown. The major promise therefore lies in understanding the pathophysiology of newly identified genes with the perspective of novel therapeutic approaches.
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43

Eckardstein, Arnold von, and Dimitris Kardassis. High Density Lipoproteins: From Biological Understanding to Clinical Exploitation. Springer, 2015.

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44

Eckardstein, Arnold von, and Dimitris Kardassis. High Density Lipoproteins: From Biological Understanding to Clinical Exploitation. Springer, 2016.

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45

Jacobson, Marc. Atherosclerosis Prevention: Identification and Treatment of the Child with High Cholesterol (Monographs in Clinical Pediatrics). Routledge, 1991.

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46

Tulenko, Thomas N. Recent Advances in Arterial Diseases: Atherosclerosis, Hypertension and Vasospasm (Progress in Clinical and Biological Research). Wiley-Liss, 1986.

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47

Vlachopoulos, Charalambos, and Nikolaos Ioakeimidis. Erectile dysfunction as a marker and predictor of cardiovascular disease. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0245.

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Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.
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48

Jood, Katarina, and Turgut Tatlisumak. Special aetiologies. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0006.

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The chapter ‘Special aetiologies of ischaemic stroke in young adults’ provides an overview of the broad spectrum of non-conventional causes of ischaemic stroke. It reviews the more common of these unusual conditions categorized as non-atherosclerotic non-inflammatory arteriopathies, non-atherosclerotic inflammatory arteriopathies, vasospastic syndromes, haematological disorders, genetic disorders, and miscellaneous disorders. It discusses strategies for aetiological diagnosis in young ischaemic stroke, provides a detailed overview of useful clinical clues obtained from patient history and physical examinations, and describes a patient-tailored step-wise diagnostic strategy based on clinical clues and findings from a group of basic diagnostic tests.
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49

Diehm, C., and H. Sinzinger. Prostaglandin E1: New Aspects on Pharmacology, Metabolism and Clinical Efficacy. Springer, 1992.

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50

Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0213.

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Renovascular disease refers to a narrowing of a main or branch renal artery. Consequences include loss of functional renal tissue and renovascular hypertension, with other manifestations depending on the underlying cause. Worldwide the most common cause is atherosclerotic narrowing, with other causal pathologies including fibromuscular disease (FMD) and inflammatory conditions. FMD occurs much more frequently in women than in men, and is associated with smoking but genetic predisposing factors are also suspected. In South East Asia, Takayasu arteritis is an important cause.Takayasu disease often presents in a non-specific syndromic manner with fatigue and malaise. FMD often presents with early-onset hypertension. Atherosclerotic renal artery stenosis is often clinically silent with suspicion raised due to the existence of other cardiovascular pathology with the more dramatic presentations of acute decompensated heart failure or acute kidney injury less common. Clinical criteria can identify patients at risk.
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