Carotid atherosclerosis

Patients with arterial disease caused by atherosclerosis, carotid, coronary, aortic, or LEAD are prone to thrombosis. 

SALONEN J T, YLA-HERTTUALA S, YAMAMOTO R, BUTLER S, KORPELA H, SALONEN R, NYYSSONEN K, PALiNSKi w, wiTZTUM J L (1992) Autoantibody against oxidised LDL and progression of carotid atherosclerosis, Lancet, 339, 883-7. 

SALONEN J T, NYYSSONEN K, SALONEN R, PORKKALA-SARATAHO E, TUOMAINEN T P, DICZFALUSY U, BJORKHEM I (1997) Lipoprotein oxidation and progression of carotid atherosclerosis, Circulation, 95, 840—45. 

Carotenoids and cardiovascular diseases — Numerous epidemiological studies aimed to study the relationship of carotenoids and cardiovascular diseases (CVDs) including coronary accident risk and stroke. It appeared then that observational studies, namely prospective and case-control studies, pointed to a protective effect of carotenoids on myocardial infarct and stroke, but also on some atherosclerosis markers such as intima media thickness (IMT) of the common carotid artery (CCA) and atheromatous plaque formation. 

Bonithon-Kopp, C. et al.. Combined effects of lipid peroxidation and antioxidant status on carotid atherosclerosis in a population aged 59-71 years The EVA (Etude sur le Vieillisement Arteriel) study. Am. J. Clin. Nutr, 65, 121, 1997. 

Iribarren, C. et al.. Association of serum vitamin levels, LDL susceptibility to oxidation, and autoantibodies against MDA-LDL with carotid atherosclerosis a case-control %Vady, Arterioscler. Thromb. Vase. Biol, 17, 1171, 1997. 

Andrews, B., Rice-Evans, C., Paganga, G., Leake, D., Bumand, K., Browse, N., Sommerville, K. and Taub, N. (1994). Oxidisability of low density lipoproteins in patients with carotid or femoral atherosclerosis. Atherosclerosis (in press). 

The basic biology of chemokines and their receptors is well covered in Chapters 2 and 3 of this book, and we will focus hereafter upon the roles of individual chemokines and receptors in atherosclerosis. The largest amount of data on the roles of chemokines in cardiovascular disease (C VD) has been obtained from in vitro studies and murine models, which will be discussed in detail. In man, genetic polymorphisms in chemokine and chemokine-receptor genes have pointed to an important role for specific chemokines in various atherosclerotic diseases including coronary artery disease and carotid artery occlusive disease. For properties see Table 1. 

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. 

Rissanen TH, Voutilainen S, Nyyssonen K, Salonen R, Kaplan GA and Salonen JT. 2003. Serum lycopene concentrations and carotid atherosclerosis The Kuopio Ischaemic Heart Disease Risk Factor Study. Am J Clin Nutr 77(1) 133-138. 

In carotid atherosclerosis, plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or may dislodge and travel distally, eventually occluding a cerebral vessel. 

Only fragmentary information exists in the human. In a study on 27 postmenopausal women with breast cancer, tamoxifen slightly slowed the progression of atherosclerosis as assessed by changes in carotid intima-media thickness (Stamatelopoulos et al. 2004). 

Ceresini G, Marchini L, Rebecchi I, Morganti S, Bertone L, Montanari I, Bacchi-Modena A, Sgarabotto M, Baldini M, Denti L, Ablondi F, Ceda GP, Valenti G (2003) Effects of raloxifene on carotid blood flow resistance and endothelium-dependent vasodilation in postmenopausal women. Atherosclerosis 167 121-127... 

Hwang SJ, Ballantyne CM, Sharrett AR, Smith LC, Davis CE, Gotto AM Jr, Boerwinkle E (1997) Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases the Atherosclerosis Risk In Communities (ARIC) study. Circulation 96 4219-4225... 

In addition to coronary sclerosis, evidence is accumulating that high Lp(a) levels may be important in the development of cerebrovascular and peripheral arterial disease, as well (J6, T8, U2). Lp(a) levels not only correlated well with clinical endpoints such as transient ischemic attack and cerebral infarction, but also were associated with the extent and severity of carotid atherosclerosis, as assessed by bidirectional Doppler ultrasound (K23, M33, Z2). 

J6. Joviiic, A., Ivanisevic, V., and Ivanovic, I., Lipoprotein(a) in patients with carotid atherosclerosis and ischemic cerebrovascular disorders. Atherosclerosis (Shannon, Irel.) 98, 59-65 (1993). 

T4. Tato, F., Keller, C., Schuster, H., Spengel, F., Wolfram, G., and Zollner, N., Relation of lipoprotein(a) to coronary heart disease and duplex sonographic findings of the carotid arteries in heterozygous and familial hypercholesterolemia. Atherosclerosis (Shannon. Irel.) 101, 69-77 (1993). 

Increasing Oxygen. It was once believed that the cause of Alzheimer s dementia was poor oxygen snpply to the brain. This theory suggested that atherosclerosis, hard plaques of fat and calcium, accumulate in blood vessels and block the arteries that snpply the brain, depriving it of oxygen-rich blood. In fact, atherosclerosis does occnr in the carotid arteries that snpply the brain and is the most common cause of stroke and vascnlar dementia. There is no evidence that this mechanism is involved in the pathology of Alzheimer s disease. 

Martin, H., and Abraham, D. (2005). Visual vignette. Unilateral carotid vascular atherosclerosis. Endocr. Pract. 11,352. 

Additionally, human studies of atherosclerosis, mainly located in the carotid ateries and thoratic aorta, with p FlFDO PET were performed. These investigations strengthen the status of p FJEDG PET as noninvasive plaque-imaging technique [191-196]. 

Heterozygous carriers of functionally relevant mutations usually present with HDL cholesterol levels that are frequently below the fifth percentile. As would be expected, apoA-I levels are also frequently below the fifth percentile (i.e., < 1.05 g/1 and < 1.1 g/1 in Caucasian men and women, respectively). In most cases, heterozygous carriers of apoA-I variants do not present with specific clinical symptoms. An important exception are some structural apoA-I variants with amino acid substitutions in the amino terminus, which have been detected in patients with familial amyloidosis of the liver, the intestine, the kidney, the heart, peripheral nerves, and in the skin. In addition, some apoA-I variants like apoA-I L178P or L159P have been associated with increased risk of premature coronary heart disease or enhanced progression of carotid intima media thickness, whereas others did not show this association, or were even claimed to have reduced cardiovascular risk and advocated as possible agents for the treatment or prevention of atherosclerosis (notably apoA-I R173CMiiano) [22,43,53]. 

It has been hypothetically suggested that the use of HRT could slow the progression of atherosclerosis by an effect on lipids. In a 1-year study of 321 women with increased thickness of the carotid intima media who were using either various forms of HRT or none at all, there was no slowing in the progression of subclinical atherosclerosis and no unfavorable effect on the process (23). HRT significantly reduced LDL cholesterol, fibrinogen, and FSH. 

Concentrations of lipoprotein(a) were measured in 51 patients taking long-term carbamazepine, phenobarbital, phenytoin, or valproate and 51 age- and sex-matched controls (133). Lipoprotein(a) concentrations were above 450 pg/ml in 11 patients compared with only 4 controls, and the mean serum lipoprotein(a) concentrations were 330 and 169 pg/ml respectively. The epileptic patients also had a thicker intima media of the common carotid artery. These results suggest that patients taking antiepileptic drugs may be at a higher risk of atherosclerosis. 

Atherosclerosis is a pathogenic response of the intima of the arterial vessel walls to noxious stimuli. It is characterized by lipids depositing in the vessel walls, which leads to wall narrowing. This can progress to IHD. Exposure to arsenic in drinking water is associated with an increased prevalence of carotid atherosclerosis in a dose-response relationship. In a cross-sectional study, Wang et al. (2002) assessed... 

Wang, C.-H., Jeng, J.-S., Yip, P.-K. el al. (2002) Biological gradient between long-term arsenic exposure and carotid atherosclerosis. Circulation, 105(15), 1804-9. 

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