Atherosclerosis: Diet and Drugs by Arnold Eckardstein

By Arnold Eckardstein

This ebook supplies an summary on very important mechanisms interested in atherosclerosis and thereby provides objectives a few of that are used and others that could be necessary for remedy and prevention of atherosclerosis. considering atherosclerosis is a multifactorial illness the scientifc procedure needs to be multidisciplinary. consequently, the authors of this publication signify various components of technique starting from easy, medical and inhabitants study in addition to diverse fields of workmanship starting from metabolism to immunology and irritation biology and to vascular biology.

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Thrombi arising due to plaque rupture often fill large areas within the plaque and may be surrounded or infiltrated by areas of haemorrhage. Haemorrhagic events occur frequently in advanced atherosclerotic lesions either by infiltration of blood from the lumen through fissures or by rupture or by degradation of vasa vasora which frequently grow at the plaque base (Kolodgie et al. 2003). Due to the high thrombogenicity of the plaque base, intra-plaque haemorrhages are usually subject to clotting and undergo essentially the same fate as lumenal thrombi.

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. About 10 years ago, a paradigm shift occurred when it was realized that the severe and sometimes fatal complications of atherosclerosis do not necessarily take place in those with the heaviest burden of disease.

The site of action of these drugs may be the key to explaining the beneficial effects. 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.

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