Atherosclerosis: Diet and Drugs by Arnold Eckardstein

By Arnold Eckardstein

This booklet offers an outline on vital mechanisms thinking about atherosclerosis and thereby offers goals a few of that are used and others that could be helpful for remedy and prevention of atherosclerosis. considering atherosclerosis is a multifactorial disorder the scientifc procedure has to be multidisciplinary. for that reason, the authors of this publication signify diversified components of method starting from simple, 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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Extra resources for Atherosclerosis: Diet and Drugs

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In most cases, the thrombus does not occlude the artery but is organized and incorporated into the vessel wall, thus contributing to the growth of the atherosclerotic plaque. According to Renu Virmani and her colleagues (Virmani et al. 2000), thrombus may form at the site of atherosclerosis for three reasons: 1. Rupture of the cap or shoulder of a thin fibrous cap may lead to direct contact of the highly thrombogenic core with the blood stream. 2. Erosion of the endothelial layer exposes the subendothelial collagenous matrix of the intima to the bloodstream.

Three types of calcification are recognized in vascular tissue: cardiac valve calcification, calcification of the intimal layer associated with atherosclerosis and calcification of the tunica media (Mönckeberg calcification), which is associated with electrolyte disturbances or with metabolic disorders such as vitamin D poisoning, end-stage renal failure and diabetes mellitus. Medial calcification tends to affect arteries such as those of the abdominal viscera or the arms that are less prone to develop atherosclerosis and has never been reported in coronary arteries.

1 Role of Mast Cells in Recruitment of Inflammatory Cells Adhesion of circulating monocytes to the endothelium is one of the earliest steps in atherosclerosis (Li et al. 1993). Their entry into the arterial intima depends on the interaction with adhesion molecules on the surface of the endothelium. Activated mast cells secrete a variety of pro-inflammatory substances (Bradding 1996), many of which, such as TNFα, tryptase and histamine (Burns et al. 1999; Compton et al. 2000; Pober et al. 1986), cause endothelial cells to express adhesion molecules such as P-selectin and VCAM-1, which are responsible for the recruitment of monocytes and lymphocytes.

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