Lipids and atherosclerosis annual 2001 by Gaw, Allan; Shepherd, James PDF

By Gaw, Allan; Shepherd, James

ISBN-10: 0203213092

ISBN-13: 9780203213094

ISBN-10: 0203270169

ISBN-13: 9780203270165

ISBN-10: 0203291255

ISBN-13: 9780203291252

ISBN-10: 1853179043

ISBN-13: 9781853179044

Given the ongoing improvement of latest statins and their expanding, worthy use in medical perform and given the significance of scientific examine into the atherosclerotic plaque and its position in cardiovascular and endovascular ailments, given the gigantic advances in animal and human experiences that experience taken position over the last few years at a progressively expanding velocity, Gaw and Shepherd have selected issues on lipids Read more...

summary: Given the ongoing improvement of latest statins and their expanding, invaluable use in medical perform and given the significance of scientific study into the atherosclerotic plaque and its function in cardiovascular and endovascular ailments, given the substantial advances in animal and human reports that experience taken position over the last few years at a gradually expanding velocity, Gaw and Shepherd have selected issues on lipids and atherosclerosis, that are of present curiosity for researchers and clinicians alike. for this reason, the necessity for a widespread up to date evaluation of those advances is apparent

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Example text

They also add weight to the idea that statin therapy has an antiinflammatory plaque-stabilizing effect, which could be independent of its lipid-lowering action. The balance of atherosclerosis: therapeutic implications Atherosclerosis is a dynamic process in which the balance between the destructive influence of inflammatory cells and the reactive, stabilizing effects of VSMCs determines outcome (Fig. 2). The balance is tipped in favour of plaque rupture by factors such as an atherogenic lipoprotein profile, extent of lipid oxidation, local free radical generation, and genetic variability in expression and activity of the inflammatory molecules involved.

NO is a potent vasodilator of all classes of blood vessels. It also has a number of other actions that can be thought of as antiatherogenic. For example, it is a powerful inhibitor of platelet aggregation on endothelial cells. 8 This may occur either because of endothelial cell dysfunction, or as a consequence of increased NO breakdown. 20 Many atherosclerosis risk factors are associated with impaired endothelial function, mediated through a reduction in the capacity to produce NO. For example, in hyperlipidaemic patients, forearm bloodflow was measured in response to serotonin-induced vasodilatation, an index of NO-dependent vasodilatation.

33 T-cells are of the T-helper type 1 class, characterized by the production of interleukin-2 and interferon gamma (IFN-γ). These factors can alter plaque morphology, and can also upregulate adhesion molecule expression on endothelial cells, and thus recruit more cells to join the inflammatory process. It is now generally recognized that the progression and consequences of atherosclerosis are determined by dynamic interactions between inflammatory cells recruited in response to subendothelial lipid accumulation and the local reparative ‘wound-healing’ response of surrounding VSMCs.

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Lipids and atherosclerosis annual 2001 by Gaw, Allan; Shepherd, James


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