Atherosclerotic lesions carotid

In Apo E-deficient animals fed a normal chow diet, fatty streaks are first observed in the proximal aorta at 10 to 12 weeks (15). The xanthoma that forms in the intima contains foam cells and is often called the early atherosclerotic lesion and is critically dependent on monocytes. Smooth muscle cells (SMCs) arrive in the intima at approximately 15 weeks and form a fibrous cap around 20 weeks (16). By 36 weeks, lumen narrowing occurs in the external branches of the carotid artery (incidence -75%), but the lumen size is maintained in the aorta. Lumen narrowing, or stenosis, does not correlate with plaque size but... 

The presence of atherosclerotic lesions on duplex scanning of the carotid arteries in FH patients, has recently been associated with increased Lp(a) concentrations (T4), and Sorensen et al. (S39) demonstrated a relationship between... 

Figure 8.1 Therapeutic effect of pomegranate juice on atherosclerotic lesion area in E° mice (A-C) or in patients with carotid artery stenosis (D and E). Thirty E° mice and 10 patients with severe CAS were supplemented with PJ concentrate (12.5 pL/mouse/day and 50 mL/day, respectively) for 9 weeks or for 1 year, respectively. Photomicrographs of typical foam cells from unsupplemented 4-month-old E° mice and from 6-month-old E° mice administered a placebo (B) or PJ (C) are presented. Mean ( SEM) effect of PJ consumption on human common carotid artery IMT (D) and end diastolic velocity (EDV) (E) are shown. = p < 0.01 (after vs. before PJ consumption).

Studies of plasma homocysteine and the thickness of atherosclerotic lesions or of the diameter of the coronary artery or the carotid artery. 

Fig. 13 Coronal tomographic image of a patient with carotid atherosclerotic lesions obtained 4h after IV administration of In-111 labeled negative-charge modified murine-human chimeric Z2D3 F(ab )2 (B). The arrow denotes the carotid lesion. (A) The crotid angiogram demonstrating a severe right internal carotid artery lesion (arrow) is shown.

A study of 1401 subjects involved measuring plasma homocysteine and measuring the lesions in the carotid artery, one of the arteries in the body that tends to acquire atherosclerotic lesions. The thickness of the lesions were measured by ultrasonography. Plasma folate, vitamin Bg, and vitamin B12 were also measured. A correlation was found between narrowing of the artery and homocysteine levels at above 15 xM homocysteine. A correlation with narrowing of the artery was also found with folate levels below 2.5 ng/ml, and with vitamin Bg levels below 30 nM (Selhub et al, 1995). A study of 231 normal subjects and 304 patients with atherosclerosis (coronary artery under 30% normal diameter) revealed a striking correlation between plasma homocysteine of 12 pM, or greater, and atherosclerosis (Robinson et al, 1995). These studies help define an upper limit of acceptable plasma homocysteine levels. 

Aviram M, Hardak E, Vaya J, et al. Human serum paraoxonases (PONI) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions. Circulation 2000 101 2510-2517. 

Growing clinical data also points to the importance of IL-8 in atherogenesis. IL-8 has been found in atheromatous lesions from patients with atherosclerotic disease including carotid artery stenosis (103), CAD (118), abdominal aortic aneurysms (AAA) (103,104,114), and peripheral vascular disease (PVD) (104). Furthermore, studies using plaque explant samples have yielded more direct evidence for IL-8 involvement. Media from cultured AAA tissue induced IL-8-dependent human aortic endothelial cell (HAEC) chemotaxis (122). Homocysteine, implicated as a possible biomarker for CAD, is also capable of inducing IL-8 (123-125) by direct stimulation of endothelial cells (123,124) and monocytes (125). When patients with hyperhomocysteinemia were treated with low-dose folic acid, decreases in homocysteine levels correlated with decreases in IL-8 levels (126). Statins significantly decrease serum levels of IL-6, IL-8, and MCP-1, as well as expression of IL-6, IL-8, and MCP-1 mRNA by peripheral blood monocytes and HUVECs (127). Thus, IL-8 may be an underappreciated factor in the pathogenesis of atherosclerosis. 

Yuan C, Mitsumori LM, Beach KW et al. (2001) Carotid atherosclerotic plaque noninvasive MR characterization and identification of vulnerable lesions. Radiology 221 285-299... 

The level of oxidative protein modifications may indicate oxidative stress in normal and pathological conditions. Increased content of carbonyl groups was found in diffusely thickened intima (neointima) of arterial walls in arteriosclerotic tissues (M19). Comparison of oxidatively modified amino acids content in normal intima and in human carotid plaque samples revealed an increased content of 3-chlorotyrosine, DOPA, o-tyrosine, m-tyrosine, hydroxyleucine, hydroxyva-line, and especially, dityrosine (F17, H13). These plaques are indicative of the role of protein oxidative damage in the formation of atherosclerotic plaques. Postmortem studies revealed that the content of dityrosine is increased in the stage of advanced lesions. However, the o-tyrosine and m-tyrosine are not elevated in plaque proteins (H13, LI 1). The question of 3-nitrotyrosine level in atherosclerotic plaques remains unresolved, the reported data being contradictory (E6, L10, M24). 

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