Relevant bibliographies by topics / Atherosclerosis – Risk factors / Books
To see the other types of publications on this topic, follow the link: Atherosclerosis – Risk factors.

Books on the topic 'Atherosclerosis – Risk factors'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 books for your research on the topic 'Atherosclerosis – Risk factors.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Maciejko, James J. Atherosclerosis Risk Factors. Washington, DC: AACC Press, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

M, Grundy Scott, and Current Medicine Inc, eds. Atlas of atherosclerosis. 4th ed. Philadelphia: Current Medicine, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

1948-, Wilson Peter, and Current Medicine Inc, eds. Atlas of atherosclerosis: Risk factors and treatment. 3rd ed. Philadelphia: Current Medicine, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tousoulis, Dimitris. Risk factors and vascular endothelium. Hauppauge, N.Y: Nova Science Publishers, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zhang, Xiao-hua. Investigations of effects of garlic materials upon risk factors of atherosclerosis. Wolverhampton: University of Wolverhampton, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schettler, Gotthard, ed. Endemic Diseases and Risk Factors for Atherosclerosis in the Far East. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83358-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Yeagle, Philip. Understanding your cholesterol. San Diego: Academic Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yeagle, Philip. Understanding your cholesterol. San Diego: Academic Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

M, Gotto Antonio, ed. Multiple risk factors in cardiovascular disease. Dordrecht: Kluwer Academic Publishers, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Frank, Clifford R. Pediatric prevention of atherosclerotic cardiovascular disease. New York: Oxford University Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
11

Wu, James T. Early risk assessment of cancer and atherosclerosis: Identification of common risk markers, and preventive nutrition. Washington, DC: AACC Press, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
12

Mangiapane, E. H. Diet, lipoproteins andcoronary heart disease: A biochemical perspective. Nottingham: Nottingham University Press, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
13

1922-, Berenson Gerald S., and Bogalusa Heart Study, eds. Causation of cardiovascular risk factors in children: Perspectives on cardiovascular risk in early life. New York: Raven Press, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
14

The lipid hypothesis of atherogenesis. Austin: R.G. Landes, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
15

Bernard, Pacaud, ed. La cocina de sus arterias. Barcelona: De Vecchi, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
16

1947-, Lusis Aldons J., Rotter Jerome I, and Sparkes Robert S. 1930-, eds. Molecular genetics of coronary artery disease: Candidate genes and processes in atherosclerosis. Basel: Karger, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
17

Mangiapane, E. H. Diet, lipoproteins and coronary heart disease: A biochemical perspective. Nottingham: Nottingham University Press, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
18

M, Forte Trudy, ed. Hormonal, metabolic, and cellular influences on cardiovascular disease in women. Armonk, NY: Futura Pub., 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
19

The beauty of the cross: The passion of Christ in theology and the arts, from the catacombs to the eve of the Renaissance. New York: Oxford University Press, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
20

Viladesau, Richard. The beauty of the cross: The passion of Christ in theology and the arts, from the catacombs to the eve of the Renaissance. Oxford: Oxford University Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
21

Atherosclerosis: Risk Factors & Treatment. Mosby-Year Book, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
22

Virgil, Brown W., ed. Atherosclerosis: Risk factors and treatment. St. Louis: Mosby, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
23

Wilson, Peter W. F. Atlas of Atherosclerosis. 2nd ed. Current Medicine, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
24

Sakamoto, Hayato, and Etsuo Murakami. Atherosclerosis: Risk Factors, Prevention and Treatment. Nova Science Publishers, Incorporated, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
25

Grundy, Scott M. Atlas of Atherosclerosis : Risk Factors and Treatment. 4th ed. Current Medicine Group, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
26

Wilson, Peter W. F. Atlas of Atherosclerosis: Risk Factors and Treatment. Current Medicine Group LLC, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
27

Atlas of Atherosclerosis: Risk Factors and Treatment. 2nd ed. Current Medicine Group, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
28

Wilson, Peter W. F. Atlas of Atherosclerosis: Risk Factors and Treatment. Current Medicine Group LLC, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
29

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
30

Braunwald, Eugene. Atlas of Atherosclerosis and Metabolic Risk Syndrome: Risk Factors and Treatment. Current Medicine Group, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
31

Endemic diseases and risk factors for atherosclerosis in the Far East. Berlin: Springer-Verlag, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
32

Schettler, Gotthard. Endemic Diseases and Risk Factors for Atherosclerosis in the Far East. Springer, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
33

Gotto, Antonio M. Multiple Risk Factors in Cardiovascular Disease. Ingramcontent, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
34

Focus On Atherosclerosis Research. Nova Science Publishers, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
35

(Editor), Michel E. Safar, and Edward D. Frohlich (Editor), eds. Atherosclerosis, Large Arteries and Cardiovascular Risk (Advances in Cardiology). S. Karger AG (Switzerland), 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
36

Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.

Full text
Abstract:
This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages. Progression from stable coronary plaques to the plaque rupture that underlies the acute coronary syndrome is discussed in detail. The chapter provides a basic up-to-date concept of the development and progression of atherosclerosis and highlights the stages where preventive measures may still be effective.
APA, Harvard, Vancouver, ISO, and other styles
37

Selected risk factors and carotid artery plaque in men with heart disease. 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
38

Selected risk factors and carotid artery plaque in men with heart disease. 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
39

Graham, Ian, Therese Cooney, and Dirk De Bacquer. Risk stratification and risk assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0005.

Full text
Abstract:
Cardiovascular disease (CVD) is the biggest cause of death worldwide. The underlying atherosclerosis starts in childhood and is often advanced when it becomes clinically apparent many years later. CVD is manageable: in countries where it has reduced this is due to changes in lifestyle and risk factors and to therapy. Risk factor management reduces mortality and morbidity. In apparently healthy people CVD risk is most frequently the result of multiple interacting risk factors and a risk estimation system such as SCORE can assist in making logical management decisions. In younger people a low absolute risk may conceal a very high relative risk, and use of the relative risk chart or calculation of their ‘risk age’ may help in advising them of the need for intensive life style efforts. All risk estimation systems are relatively crude and require attention to qualifying statements.
APA, Harvard, Vancouver, ISO, and other styles
40

Lamb, Hildo J. Visceral and Ectopic Fat: Risk Factors for Type 2 Diabetes, Atherosclerosis, and Cardiovascular Disease. Elsevier, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
41

Visceral and Ectopic Fat: Risk Factors for Type 2 Diabetes, Atherosclerosis, and Cardiovascular Disease. Elsevier, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
42

Cardiovascular Risk Factors, An Issue of Clinics in Laboratory Medicine. Saunders, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
43

Atlas Of Atherosclerosis And Metabolic Syndrome. Springer, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
44

Grundy, Scott M. Atlas of Atherosclerosis and Metabolic Syndrome. Springer, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
45

Grundy, Scott M. Atlas of Atherosclerosis and Metabolic Syndrome. Springer New York, 2016.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
46

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

Full text
Abstract:
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 ...
APA, Harvard, Vancouver, ISO, and other styles
47

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

Full text
Abstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
APA, Harvard, Vancouver, ISO, and other styles
48

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

Full text
Abstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
APA, Harvard, Vancouver, ISO, and other styles
49

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

Full text
Abstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
APA, Harvard, Vancouver, ISO, and other styles
50

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Atherosclerosis – Risk factors' for other source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography