Fibrous plaques, atherosclerosis

Smith, E. B., and Cochran, S., Factors influencing the accumulation in fibrous plaques of lipid derived from low-density lipoprotein II. Preferential immobilization of lipoprotein(a) [Lp(a)]. Atherosclerosis (Shannon, Irel.) 84, 173-181 (1990). 

The interactions of these cells with T lymphocytes also in the lesion and the overlying endothelium can lead to a massive flbroproliferative response over which connective tissue from smooth muscle cells form a fibrous cap. This covers the advanced lesion or fibrous plaque of atherosclerosis, deeper portions of which consist of macrophages, T lymphocytes, smooth muscle cells, connective tissue, necrotic debris and varying amounts of lipids and lipoproteins. 

Atherosclerosis involves the formation of lipid-rich plaques in the intima of arteries. The plaques begin as fatty streaks containing foam cells, which initially are macrophages filled with lipids, particularly cholesterol esters. These early lesions develop into fibrous plaques that may occlude an artery and cause a myocardial infarct or a cerebral infarct. Formation of these plaques is often associated with abnormalities in... 

In susceptible populations atherosclerosis may start quite early in life. Early (fatty streak) lesions may be seen during the second decade of life and fibrous plaques during the third. These primary pathological changes in arteries therefore antedate, by at least twenty years, the appearance of symptoms above the clinical horizon (Bierman, 1973). In virtually all the populations studied this far, the presence of lesions and the morbidity attributable to underlying atherosclerosis is much more frequent in males than females and at any given age men have more severe coronary artery disease than women. 

Harman, D. Atherosclerosis possible role of serum copper in the conversion of fatty streaks to fibrous plaques. 

Atherosclerosis is main cause of cardiovascular deaths. It is characterized by a localised plaque in the intima and is composed of cholesterol esters, deposition of fibrous proteins and calcification. These plaques may narrow the arterial lumen and can cause distalischemia. The coronary and cerebral circulation are main sites of atherosclerosis. Raised levels of VLDL, LDL... 

Furthermore, Ang n has been found to contribute to VSMC senescence, which has been implicated in the pathogenesis of atherosclerosis (Kunieda et al. 2006). Cell senescence may promote plaque instability, since loss of VSMCs leads to transformation into a rupture-prone plaque with a thin fibrous cap over the lipid-rich core (Geng and Libby 2002). 

Complications of atherosclerosis are the leading cause of morbidity and mortahty in developed countries. It can be considered as a chronic inflammation resulting from interaction between modified lipoproteins, monocyte-derived macrophages, T cells, and the normal cellular elements of the arterial wall [107-109]. The earliest lesion is a pure inflammatory lesion consisting of monocyte-derived macrophages and T cells. The presence of monocytes in every phase of atherosclerosis, and of hydrolytic enzymes secreted by these and other cells, play a central role in different stages of the disease, particularly in the resorption of the fibrous cap leading to plaque rupture. 

Many animal cells take up cholesterol through receptor-mediated endocytosis and In this way acquire most of the cholesterol they require to make new membrane. If the uptake Is blocked, cholesterol accumulates In the blood and can contribute to the formation In blood vessel walls of atherosclerotic plaques - the deposits of lipid and fibrous tissue that cause strokes and heart attacks by blocking blood flow. In fact, It was through a study of humans with a strong genetic predisposition for atherosclerosis that the mechanism of receptor-mediated endocytosis was first clearly revealed. 

Introduction - Atherosclerosis is defined by the WHO "as a variable combination of changes of the intima of arteries consisting of the focal accvimulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposits and associated with medial changes." Once formed the advanced plaque seldom regresses, and consequently major research attention has concentrated on prevention of additional deposits or, in the longer view, on the primary prevention of all lesions. 

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