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 booklet provides an outline on vital mechanisms serious about atherosclerosis and thereby offers goals a few of that are used and others that may be valuable for remedy and prevention of atherosclerosis. considering that atherosclerosis is a multifactorial affliction the scientifc method has to be multidisciplinary. for that reason, the authors of this e-book characterize assorted components of technique starting from simple, scientific and inhabitants examine in addition to assorted fields of craftsmanship starting from metabolism to immunology and irritation biology and to vascular biology.

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Christ et al. showed that smooth muscle cells from atherosclerotic vessels produce less tissue plasminogen activator and more plasminogen activator inhibitor than smooth muscle cells from normal vessels (Christ et al. 1997). Why did evolution allow development of an apparently self-destructive mechanism whereby thrombus formation leads to growth of the atherosclerotic plaque? Russell Ross once called atherosclerosis ‘a defence mechanism gone awry’ (Ross 1981). This idea fits very well to the thrombotic process in atherosclerosis.

In particular, the importance of calcification lies in the stratification of risk in asymptomatic patients at intermediate risk of coronary heart disease, in whom the calcium score appears to provide information over and above that provided by conventional risk factors. 4 From Lesion to Infarction: The Vulnerable Plaque Until quite recently, it was assumed that the risk of myocardial infarction, stroke or sudden coronary death was related simply to the total burden of atherosclerotic disease: the greater the extent of atherosclerosis, the higher the event risk.

It is generally accepted that intimal smooth muscle cells are mainly involved in building up the fibrous cap and in synthesizing the collagenous matrix that provides its tensile strength. Invasion of macrophages is believed to weaken the cap by secretion of matrix-degrading enzymes such as MMP3 and MMP9 and cathepsins (Galis et al. 1994). Recent observations, however, suggest that macrophages may also be able to synthesize components of the extracellular matrix. Active collagen type I expression can be demonstrated by in situ hybridization only in smooth muscle cells in the vicinity of non-foamy macrophages (Jaeger et al.

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Atherosclerosis: Diet and Drugs by Arnold Eckardstein

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