Fibrous plaque

At cellular level each stage of atheroma development is accompanied by the expression of specific glycoproteins by endothelial cells which mediate the adhesion of monocytes and T-lymphocytes. Their recruitment and migration is triggered by various cytokines released by leukocytes and possibly by smooth muscle cells. Atheroma development continues with the activation of macrophages, which accumulate lipids and become, together with lymphocytes, so-called fatty streaks. The continuous influx, differentiation and proliferation finally leads to more advanced lesion and to the formation of the fibrous plaque. ... 

Lipid-laden macrophages, smooth muscle cells, and necrotic debris from the death of foam cells accumulate in the subendothelial space, leading to enlargement of the fatty streak. A collagen matrix forms a fibrous cap that covers the lipid core of the lesion to establish a fibrous plaque called an atherosclerotic plaque. Initially, the diameter of the coronary artery lumen is... 

Repeated injury and repair within an atherosclerotic plaque eventually lead to a fibrous cap protecting the underlying core of lipids, collagen, calcium, and inflammatory cells such as T lymphocytes. Maintenance of the fibrous plaque is critical to prevent plaque rupture and subsequent coronary thrombosis. 

IL-6 participates in both atherogenesis and inflammatory processes. In one interesting mouse model that was double deficient at the apoE and IL-6 loci, animals displayed similar hypercholesterolemia compared to apoE-null mice, but disclosed larger and more calcified lesions at 1 year of age (Klinge 2001). Thus, IL-6 appears to be involved at the fibrous plaque stage of the atherosclerotic process. Moreover, IL-6 is a key factor in the generation of the hepatic acute-phase response and so increases the levels of CRP, fibrinogen, platelet... 

As Lp(a) also binds to glycoprotein-IIb on platelets (M9), its role in formation of fibrous plaque lesions could also exist by this route. 

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. 

Pearson, T. A., Wang, A., Solez, K. and Heptinstall, R. H Clonal Characteristics of Fibrous Plaques and Fatty Streaks from Human Aortas , Am. J. Palhol. (1975) 81, 379,... 

Fig. 8.2 (A) Intravascular ultrasound (IVUS) image of a coronary artery using Revolution 45 MHz IVUS imaging catheter. (B) Plaque composition imaging using volcano VH IVUS system. Green areas represent Fibrous plaque. Yellow is fibro-fatty areas. Red is the necrotic core and white represents areas of dense calcium...

Figure 7 shows that in the human aortas we observed a significant decrease in the antioxidative enzymes activity such as superoxide dismutase and glutathione peroxidase, in the areas of atheroslerotic lesions [23]. A significant drop in the activity of both key antioxidative enzymes was seen in the intimal specimens taken from the area of fatty streaks, yet a severe decrease in the activity of these enzymes was found in those taken from the area of fibrous plaques (Figure 7). 

Consequently, in the atherosclerotic aorta accumulation of oxidized LDL and activation of LDL oxidation by C-15 lipoxygenase in the vascular wall in situ may be enhanced, and rate of enzymatic detoxification of reactive oxygen species and lipohydroperoxides in the areas of atheroslerotic lesions may be drastically decreased. All these mechanisms induced the accumulation of lipohydroperoxides in the regions of lipid streaks and fibrous plaques of atherosclerotic aorta [7,8,16] (Figure 8). 

Ferritin, 739, 741,742, 756, 760 Fetal alcohol syndrome (FAS), 250, 251 FFAs, self Free falty acids Fiber, see Dietary fiber Fibrinogen, 49,530 Fibrous plaque, 360 Filamentous phage, DN A sequencing, 954-955 Fish oils, 643... 

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... 

First described in 1743 by the French surgeon, Francois de la Peyronie, Peyronie s disease is a rare, benign connective tissue disorder involving the growth of fibrous plaques in the soft tissue of the penis. Beginning as a localized inflammation, it often develops into a hardened scar. Affecting as much as 1% of men, it may cause deformity, pain, cord-like lesions, or abnormal curvature of the penis when erect. 

The fibrous plaque, which protrudes into the lumen, is composed chiefly of cholesteryl ester-loaded smooth muscle cells proliferating in the intimal layer, surrounded by collagen, elastic fibers, and proteoglycans it is enclosed in a fibrous cap. 

The complicated lesion is associated with occlusive disease the contents of the fibrous plaque become calcified and are altered as a result of hemorrhage, cell necrosis, and mural thrombosis. 

A study involving 56 patients with 116 stents showed that neointimal thickness, neointimal vascular channel density and inflammatory ceU density were much higher when there was contact between the struts and ruptured arterial media compared with the fibrous plaque or intact fibrous capsule [30]. This study suggests that coronary stenting accompanied by damage in the arterial media increased the induction of arterial inflammation, leading to neointimal growth, and thus in-stent stenosis. 

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. 

Arterial fatty streaks are ubiquitous in humans and appear early in life. The fatty streak is comprised of lipid-rich macrophages and smooth muscle cells. Macrophages that accumulate lipid and are transformed into foam cells may be involved in the transformation of the fatty streak to an atherosclerotic lesion. In susceptible persons the fatty streaks may progress to fibrous plaques. Fibrous plaques, at their core, consist of a mixture of cholesterol-rich smooth muscle and foam cells. This core may contain cellular debris, cholesteryl esters, cholesterol crystals, and calcium. The fibrous cap consists of smooth muscle and foam cells, collagen, and Hpid. The final stage in this process is the compHcated plaque, which can obstruct the arterial lumen. Rupture of the cap may lead to clot formation and occlusion of the artery. 

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