Read e-book online Atherosclerosis: Diet and Drugs PDF

By Arnold Eckardstein

ISBN-10: 3540225692

ISBN-13: 9783540225690

ISBN-10: 3540276610

ISBN-13: 9783540276616

This e-book offers an outline on vital mechanisms fascinated by atherosclerosis and thereby provides ambitions a few of that are used and others that may be necessary for remedy and prevention of atherosclerosis. considering that atherosclerosis is a multifactorial illness the scientifc procedure needs to be multidisciplinary. for that reason, the authors of this ebook signify varied parts of method starting from simple, scientific and inhabitants examine in addition to various fields of workmanship starting from metabolism to immunology and irritation biology and to vascular biology.

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Extra info for Atherosclerosis: Diet and Drugs

Example text

Nevertheless, D. N. Kim observed formation of plaques in coronary arteries of pigs on a hyperlipidaemic diet preferably at locations of pre-existing intimal thickening (Kim et al. 1987). In hypercholesterolaemia in humans, lipids tend to be deposited in the intima in the vicinity of proteoglycans (Kovanen and Pentikainen 1999). Interaction with invading monocytes/macrophages leads to oxidation of LDL which provokes foam cell formation and accumulation and, via interaction with T lymphocytes, induction of an inflammatory process (Hansson 1997).

Such ruptures recur over many years, but do not usually cause complete occlusion of the vessel, resulting instead in mural thrombi that are incorporated into the lesion. Accordingly, rupture of the atherosclerotic plaque is often clinically silent. In addition, it is important to note that thrombosis may occur at the site of an eroded atherosclerotic plaque even without a tear in the fibrous cap of the lesion (Virmani et al. 1999, 2000). There are therefore three main points that we need to remember: 1.

First, even for ACAT1 inhibitors, which suppress macrophage-associated ACAT activity, the drug’s ability to enter the lesion may be limited and moderate suppression of ACAT activity within the cells may be offset by increased cholesterol efflux. ACAT2 inhibitors, on the other hand, should have no direct effect on lesional macrophages and may turn out to be beneficial because of their ability to suppress production of atherogenic lipoproteins in the intestine (Buhman et al. 2000). 26 P. Cullen et al.

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Atherosclerosis: Diet and Drugs by Arnold Eckardstein

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