Coronary artery disease Atherosclerosis

Murr C, Winklhofer-Roob BM, Schroecksnadel K, Maritschnegg M, Mangge H, Bohm BO, Winkelmann BR, Marz M and Fuchs D. 2009. Inverse association between serum concentrations of neopterin and antioxidants in patients with and without angiographic coronary artery disease. Atherosclerosis. In press. 

A3. Abe, A., Noma, A., Lee, Y. J., and Yamaguchi, H., Studies on apolipoprotein(a) phenotypes. Part 2. Phenotype frequencies and Lp(a) concentrations in different phenotypes in patients with angiographically defined coronary artery diseases. Atherosclerosis (Shannon. Irel.) 96, 9-15 (1992). 

Ordovas JM, Civeira F, Genest J, Jr et al. Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus. Relationships with lipids, apolipopro-teins, and premature coronary artery disease. Atherosclerosis. 1991, 87 75-86. 

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Kukita H, Hiwada K, Kokubu T. Serum apolipopro-tein A-I, A-II and B levels and their discriminative values in relatives of patients with coronary artery disease. Atherosclerosis 1984 51 261-7. 

Haerem, J.W. (1972). Platelet aggregates in intramyocardial vessels of patients dying suddenly and unexpectedly of coronary artery disease. Atherosclerosis, 15, 199-213... 

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Kaneda H, Taguchi J, Ogasawara K, Aizawa T, Ohno M. Increased level of advanced oxidation protein products in patients with coronary artery disease. Atherosclerosis 2002 162 221-225. 

Tybiaerg-Hansen, A. and Humphries, S. (1992) Familial defective apolipoprotein B-100 a single mutation that causes hypercholesterolemia and premature coronary artery disease. Atherosclerosis, 96, 91. 

An increase in serum lipids is believed to contribute to or cause atherosclerosis, a disease characterized by deposits of fatty plaques on the inner walls of arteries. These deposits result in a narrowing of the lumen (inside diameter) of the artery and a decrease in blood supply to the area served by the artery. When these fatty deposits occur in the coronary arteries, the patient experiences coronary artery disease. Lowering blood cholesterol levels can arrest or reverse atherosclerosis in the vessels and can significantly decrease the incidence of heart disease. 

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. 

Iron-stimulated free radical-mediated processes are not limited to the promotion of peroxidative reactions. For example, Pratico et al. [188] demonstrated that erythrocytes are able to modulate platelet reactivity in response to collagen via the release of free iron, which supposedly catalyzes hydroxyl radical formation by the Fenton reaction. This process resulted in an irreversible blood aggregation and could be relevant to the stimulation by iron overload of atherosclerosis and coronary artery disease. 

Contrary to LDL, high-density lipoproteins (HDL) prevent atherosclerosis, and therefore, their plasma levels inversely correlate with the risk of developing coronary artery disease. HDL antiatherogenic activity is apparently due to the removal of cholesterol from peripheral tissues and its transport to the liver for excretion. In addition, HDL acts as antioxidants, inhibiting copper- or endothelial cell-induced LDL oxidation [180], It was found that HDL lipids are oxidized easier than LDL lipids by peroxyl radicals [181]. HDL also protects LDL by the reduction of cholesteryl ester hydroperoxides to corresponding hydroperoxides. During this process, HDL specific methionine residues in apolipoproteins AI and All are oxidized [182]. 

The formation of atherosclerotic plaques is the underlying cause of coronary artery disease (CAD) and ACS in most patients. Endothelial dysfunction leads to the formation of fatty streaks in the coronary arteries and eventually to atherosclerotic plaques. Factors responsible for development of atherosclerosis include hypertension, age, male gender, tobacco use, diabetes mellitus, obesity, and dyslipidemia. 

It prevents oxidation of IDL partides. Oxidized LDLs are strongly associated with atherosclerosis and coronary artery disease. 

Ila i i j i Familial hypercholesterolemia Autosomal dominant (Aa 1/500, AA 1/10 ) Cholesterol LDL High risk of atherosclerosis and coronary artery disease Homozygous condition usually death <20 years Xanthomas of the Achilles tendon Tuberous xanthomas on elbows Xanthelasmas Comeal arcus... 

This is a dominant genetic disease affecting 1/500 (heterozygous) individuals in the United States. It is characterized by elevated LDL cholesterol and increased risk for atherosclerosis and coronary artery disease. Cholesterol deposits may be seen as ... 

It is well-established that an elevated level of cholesterol, particnlarly that carried largely in the form of LDLs, is an independent risk factor for the development of atherosclerosis and its sequelae, including coronary artery disease (leading to heart attacks), strokes, and peripheral arterial disease. 

There is a mutant gene that produces an inactive receptor and patients with this mntant snffer from high levels of LDL-cholesterol in their blood. They have a markedly increased risk of developing atherosclerosis and coronary artery disease. 

Atherosclerosis and coronary heart disease are amongst the most intensively investigated subjects in medical science. Despite this, it must be pointed out that atherosclerosis is not itself a disease but a process that connibutes to diseases, such as an intermittent claudication, coronary arterial disease and stroke. 

Erkkila, A. T., Lichtenstein, A. H., Mozaffarian, D., and Herrington, D. M. (2004). Fish intake is associated with a reduced progression of coronary artery atherosclerosis in postmenopausal women with coronary artery disease. Am.. Clin. Nutr. 80, 626-632. 

The role of the antioxidant properties of vitamins C, E, and p-carotene in the prevention of cardiovascular disease has been the focus of several recent studies. Antioxidants reduce the oxidation of low-density lipoproteins, which may play a role in the prevention of atherosclerosis. However, an inverse relationship between the intake or plasma levels of these vitamins and the incidence of coronary heart disease has been found in only a few epidemiological studies. One study showed that antioxidants lowered the level of high-density lipoprotein 2 and interfered with the effects of lipid-altering therapies given at the same time. While many groups recommend a varied diet rich in fruits and vegetables for the prevention of coronary artery disease, empirical data do not exist to recommend antioxidant supplementation for the prevention of coronary disease. 

Atherosclerosis,coronary artery disease PO Initially, 20 mg/day. Maintenance 10-80 mg once daily or in 2 divided doses. Maximum 80 mg/day. 

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