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Genetic Variants and Atherosclerosis

Authors: M. Seifi, A. Ghasemi, M. Khosravi, M. Salimi, S. Jahandideh, J. Sherizadeh, F. S. Hashemizadeh, R. Khodaei

Abstract:

Atherosclerosis is the condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.

Keywords: Arterial blood vessels, atherosclerosis, cholesterol.

Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1083431

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[1] Maton, Anthea, Roshan L,et al. Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. (1993); ISBN 0-13-981176-1. OCLC 32308337
[2] Ridker PM. Inflammation, atherosclerosis, and cardiovascular risk: an epidemiologic view. Blood Coagul Fibrinolysis. 1999;10(suppl 1):S9- S12.
[3] Crouse JR, Grobbee DE, O-Leary DH, et al. Measuring effects on intima media thickness: an evaluation of rosuvastatin in subclinical atherosclerosisÔÇöthe rationale and methodology of the METEOR study. Cardiovasc Drugs Ther. 2004;18:231-238.
[4] Viles-Gonzalez JF, Fuster V, Badimon JJ. Atherothrombosis: a widespread disease with unpredictable and life-threatening consequences. Eur Heart J. 2004;25: 1197-1207.
[5] Jensen LO,Thayssen P, Pedersen KE, et al. Regression of coronary atherosclerosis by simvastatin: a serial intravascular ultrasound study. Circulation. 2004;110: 265-270.
[6] Rauch U, Osende JI, Fuster V, et al. Thrombus formation on atherosclerotic plaques: pathogenesis and clinical consequences. Ann Intern Med. 2001;134:224-238.
[7] Ohashi R, Mu H,Yao Q, et al. Atherosclerosis: immunopathogenesis and immunotherapy. Med Sci Monit. 2004; 10:RA255-RA260.
[8] Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352: 1685-1695.
[9] Ben-Haim S, Israel O. PET/CT for atherosclerotic plaque imaging. QJ Nucl Med Mol Imaging. 2006;50: 53-60.
[10] Van Mieghem CAG, McFadden EP, de Feyter PJ, et al. Noninvasive detection of subclinical coronary atherosclerosis coupled with assessment of changes in plaque characteristics using novel invasive imaging modalities. The Integrated Biomarker and Imaging Study. J Am Coll Cardiol. 2006;47:1134-1142.
[11] Weissberg PL. Atherogenesis: current understanding of the causes of atheroma. Heart. 2000;83:247-252.
[12] Carlos TM , Harlan JM. Leukocyte-endothelial adhesion molecules. Blood 1994;84:2068-101.
[13] Vora DK, Fang ZT, Liva SM, et al. Induction of P-selectin by oxidized lipoproteins. Separate effects on synthesis and surface expression. Circ Res 1997;80:810-8.
[14] Iiyama K, Hajra L, Iiyama M, et al. Patterns of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression in rabbit and mouse atherosclerotic lesions and at sites predisposed to lesion formation. Circ Res 1999;85:199-207.
[15] Gu L, Okada Y, Clinton SK, et al. Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low density lipoprotein receptordeficient mice. Mol Cell 1998;2:275-81.
[16] Watson AD, Leitinger N, Navab M, et al. Structural identification by mass spectrometry of oxidized phospholipids in minimally oxidized low density lipoprotein that induce monocyte/endothelial interactions and evidence for their presence in vivo. J Biol Chem 1997;272:13597-607.
[17] von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. Arterioscler Thromb Vasc Biol 2001; 21:13-27.
[18] Libby P, Warner SJ, Salomon RN, et al. Production of platelet-derived growth factor-like mitogen by smooth-muscle cells from human atheroma. N Engl J Med 1988;318:1493-8.
[19] Higashiyama S, Abraham JA, Miller J, et al. A heparin-binding growth factor secreted by macrophage-like cells that is related to EGF. Science 1991;251:936-9.
[20] Libby P. Changing concepts of atherogenesis. J Intern Med 2000; 247:349-58
[21] Amento EP, Ehsani N, Palmer H, et al. Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells. Arterioscler Thromb 1991;11:1223-30
[22] van der Wal AC, Becker AE, van der Loos CM, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36-44.
[23] Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994;94:2493-503.
[24] Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993;362:801- 9.
[25] Libby P. Molecular bases of the acute coronary syndromes. Circulation 1995;91:2844- 50.
[26] Davies MJ. Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. Circulation 1996; 94:2013-20.
[27] Hangartner JR, Charleston AJ, Davies MJ, Thomas AC. Morphological characteristics of clinically significant coronary artery stenosis in stable angina. Br Heart J 1986;56:501-8.
[28] Blankenhorn DH, Hodis HN (August 1993). "Atherosclerosis--reversal with therapy". The Western journal of medicine 159 (2): 172-9. PMID 8212682.
[29] Botto N, Rizza A, Colombo M, Mazzone A, Manfredi S, Masetti S, et al. Evidence for DNA damage in patients with coronary artery disease. Mutat Res 2001;493:23- 30.
[30] Andreassi MG, Botto N, Cocci F, et al. Methylenetetrahydrofolate reductase gene C677T polymorphism, homocysteine, vitamin B12, and DNA damage in coronary artery disease. Hum Genet 2003;112:171-7.
[31] Botto N, Berti S, Manfredi S, et al. Detection of mtDNA with 4977bp deletion in blood cells and atherosclerotic lesions of patients with coronary artery disease. Mutat Res 2005;570:81- 8.
[32] Henney AM, Wakeley PR, Davies MJ, et al. Localization of stromelysin gene expression in atherosclerotic plaques by in situ hybridization. Proc Natl Acad Sci USA 1991;88:8154_/8.
[33] Galis, Z.S., Khatri, J.J., 2002. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circ. Res. 90 (3), 251-262.
[34] Newby, A.C., 2005. Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. Physiol Rev. 85 (1), 1-31.
[35] Newby, A.C., Johnson, J.L., 2005. Genetic strategies to elucidate the roles of matrix metalloproteinases in atherosclerotic plaque growth and stability. Circ. Res. 97 (10), 958-960.
[36] Hayashidani, S., Tsutsui, H., Ikeuchi, M., et al. Targeted deletion of MMP 2 attenuates early LV rupture and late remodeling after experimental myocardial infarction.2003; Am. J. Physiol. Heart Circ. Physiol. 285 (3), H1229-H1235
[37] Heymans, S., Luttun, A., Nuyens, D., et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. 1999; Nature Med. 5 (10), 1135-1142.
[38] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S., Okada, Y., Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice. 2005a; J. Clin. Invest. 115 (3), 599-609.
[39] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S., Okada, Y.,. Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice. 2005b; J. Clin. Invest. 115 (3), 599-609.
[40] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection from ischemia/reperfusion injury by targeted deletion of matrix metalloproteinase-9. 2002a; Cardiovasc. Res. 54 (3), 549-558.
[41] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection from ischemia/reperfusion injury by targeted deletion of matrix metalloproteinase-9.2002b; Cardiovasc. Res. 54 (3), 549-558.
[42] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection from ischemia/reperfusion injury by targeted deletion of matrix metalloproteinase-9.2002c; Cardiovasc. Res. 54 (3), 549-558.
[43] Deschamps, A.M., Yarbrough, W.M., Squires, C.E., et al. Trafficking of the membrane type-1 matrix metalloproteinase in ischemia and reperfusion: relation to interstitial membrane type-1 matrix metalloproteinase activity. 2005; Circulation 111 (9), 1166-1174.
[44] Fedak, P.W., Smookler, D.S., Kassiri, Z., et al. TIMP-3 deficiency leads to dilated cardiomyopathy.2004; Circulation 110 (16), 2401-2409.
[45] Longo, G.M., Xiong, W., Greiner, T.C., Zhao, Y., Fiotti, N., Baxter, B.T.,. Matrix metalloproteinases 2 and 9 work in concert to produce aortic aneurysms. 2002; J. Clin. Invest. 110 (5), 625-632.
[46] Johnson, J.L., George, S.J., Newby, A.C., Jackson, C.L.,. Divergent effects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic plaque stability in mouse brachiocephalic arteries. 2005; Proc. Natl. Acad. Sci. USA 102 (43), 15575-15580.
[47] Chase, A.J., Newby, A.C.,. Regulation of matrix metalloproteinase (matrixin) genes in blood vessels: a multi-step recruitment model for pathological remodelling. 2003; J. Vasc. Res. 40 (4), 329-343.
[48] Ye S, Watts GF, Mandalia S, Humphries SE, Henney AM. Preliminary report: genetic variation in the human stromelysin promoter is associated with progression of coronary atherosclerosis. Br Heart J 1995;73:209- 15.
[49] Ye S, Eriksson P, Hamsten A, Kurkinen M, Humphries SE, Henney AM. Progression of coronary atherosclerosis is associated with a common genetic variant of the human stromelysin-1 promoter which results in reduced gene expression. J Biol Chem 1996;271:13055-60.
[50] Humphries S, Bauters C, Meirhaeghe A, Luong L, Bertrand M, Amouyel P. The 5A6A polymorphism in the promoter of the stromelysin-1 (MMP3) gene as a risk factor for restenosis. Eur Heart J 2002;23:721-5.
[51] Seifi M, Fallah S, Firoozrai M. Influence of Genetic Polymorphism in Matrix Metalloproteinase-3 on Extent of Coronary Atherosclerosis and Risk of Coronary Artery Stenosis. Archives Medical Research. In press
[52] Primo-Parmo SL, Sorenson RC, Teiber J, La Du BN. The human serum paraoxonase/arylesterase gene (PON1) is one member of a multigene family. Genomics. 1996;33:498 -507.
[53] Watson AD, Berliner JA, Hama SY, La Du BN, Faull KF, Fogelman AM, Navab M. Protective effect of high density lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J Clin Invest. 1995;96:2882-2891.
[54] Ng CJ, Wadleigh DJ, Gangopadhyay A, Hama S, Grijalva VR, Navab M, Fogelman AM, Reddy ST. Paraoxonase-2 is a ubiquitously expressed protein with antioxidant properties and is capable of preventing cellmediated oxidative modification of low density lipoprotein. J Biol Chem. 2001;276:44444-44449.
[55] Li B, Sedlacek M, Manoharan I, Boopathy R, Duysen EG, Masson P, Lockridge O: Butyrylcholinesterase, paraoxonase, and albumin esterase, but not carboxylesterase, are present in human Plasma. Biochem Pharmacol. 2005;70: 1673-1684.
[56] Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La Du BN. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions: a possible peroxidative role for praoxonase. J Clin Invest. 1998;101:1581-1590.
[57] Durrington P.N, Mackness B and Mackness M.I. Parooxonase and atherosclerosis. Arterioscler.Tromb.Vasc.Biol.2001;21:473-480
[58] Kuremoto K, Watanabe Y, Ohmura H et al: R/R genotype of human paraoxonase (PON1) is more protective against lipoprotein oxidation and coronary artery disease in Japanese subjects. J Atheroscler Thromb, 2003; 10: 85-92
[59] Huang Y, Mironova M, Lopes-Virella MF: Oxidized LDL stimulates matrix metalloproteinase-1 expression in human vascular endothelial cells. Arterioscler Thromb Vasc Biol, 1999; 19: 2640-47
[60] Navab M, Berliner JA, Watson AD et al: The yin and yang of oxidation in the development of fatty streak: a review based on the 1994 George Lyman Duff Memorial Lecture. Arterioscler Thromb Vasc Biol, 1996; 16: 831-42
[61] Navab M, Hama SY, Anantharamaiah GM et al: Normal high-density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. J Lipid Res, 2000; 41: 1495-508
[62] Mackness MI, Durrington PN: HDL, its enzymes and its potential to infl uence lipid peroxidation. Atherosclerosis, 1995; 115: 243-53
[63] Watson AD, Berliner JA, Hama SY et al: Protective effect of high density lipoprotein associated paraoxonase: inhibition of biological activity of minimally oxidized low density lipoprotein. J Clin Invest, 1995; 96: 2882-91
[64] Blatter MC, James RW, Messmer S et al: Identifi cation of a distinct human high-density lipoprotein subspecies defi ned by a lipoproteinassociated protein, K-45: identity of K-45 with paraoxonase. Eur J Biochem, 1993; 211: 871-79
[65] Kelso GJ, Stuart WD, Richter RJ et al: Apolipoprotein J is associated with paraoxonase in human plasma. Biochemistry, 1994; 33: 832-39
[66] Humbert R, Adler DA, Disteche CM et al: The molecular basis of the human serum paraoxonase activity polymorphism. Nat Genet, 1993; 3: 73-76
[67] Adkins S, Gan KN, Mody M, La du DN: Molecular basis for the polymorphic form of human serum paraoxoanase/arylesterase: glutamine or arginine at position 191, for the respective A or B allozymes. Am J Hum Genet, 1993; 52: 598-60
[68] Fortunato G, Rubba P, Panico S, Trono D, Tinto N, Mazzaccara C, De Michele M, Iannuzzi A, Vitale DF, Salvatore F, Sacchetti L. A paraoxonase gene polymorphism, PON 1 (55), as an independent risk factor for increased carotid intima-media thickness in middle-aged women. Atherosclerosis. 2003;167:141-148.
[69] Markus H, Kapozsta Z, Ditrich R, Wolfe C, Ali N, Powell J, Mendell M, Cullinane M. Increased common carotid intima-media thickness in UK African Caribbeans and its relation to chronic inflammation and vascular candidate gene polymorphisms. Stroke. 2001;32:2465-2471.
[70] Jarvik GP, Hatsukami TS, Carlson C, Richter RJ, Jampsa R, Brophy VH, Margolin S, Rieder M, Nickerson D, Schellenberg GD, Heagerty PJ, Furlong CE. Paraoxonase activity, but not haplotype utilizing the linkage disequilibrium structure, predicts vascular disease. Arterioscler Thromb Vasc Biol. 2003;1923:1465-1471
[71] Pallaud C, Sass C, Zannad F, Siest G, Visvikis S. APOC3, CETP, fibrinogen, and MTHFR are genetic determinants of carotid intimamedia thickness in healthy men (the Stanislas cohort). Clin Genet. 2001;59:316-324.
[72] Schmidt H, Schmidt R, Niederkorn K, Gradert A, Schumacher M, Watzinger N, Hartung HP, Kostner GM. Paraoxonase PON1 polymorphism leu-Met54 is associated with carotid atherosclerosis: results of the Austrian Stroke Prevention Study. Stroke. 1998;29:2043- 2048.
[73] Koch M, Hering S, Barth C, Ehren M, Enderle MD, Pfohl M. Paraoxonase1 192 Gln/Arg gene polymorphism and cerebrovascular disease: interaction with type 2 diabetes. Exp Clin Endocrinol Diabetes. 2001;109:141-145.
[74] Cao H, Girard-Globa A, Serusclat A, Bernard S, Bondon P, Picard S, Berthezene F, Moulin P. Lack of association between carotid intimamedia thickness and paraoxonase gene polymorphism in noninsulin dependent diabetes mellitus. Atherosclerosis. 1998;138: 361-366.
[75] Dessi M, Gnasso A, Motti C, Pujia A, Irace C, Casciani S, Staffa F, Federici G, Cortese C. Influence of the human paraoxonase polymorphism (PON1 192) on the carotid-wall thickening in a healthy population. Coron Artery Dis. 1999;10:595-599.
[76] Jarvik GP, Rozek LS, Brophy VH, Hatsukami TS, Richter RJ, Schellenberg GD, Furlong CE. Paraoxonase (PON1) phenotype is a better predictor of vascular disease than is PON1(192) or PON1(55) genotype. Arterioscler Thromb Vasc Biol. 2000;20:2441-2447.
[77] Leus FR, Wittekoek ME, Prins J, Kastelein JJ, Voorbij HA. Paraoxonase gene polymorphisms are associated with carotid arterial wall thickness in subjects with familial hypercholesterolemia. Atherosclerosis. 2000; 149:371-377.
[78] Sakai T, Matsuura B, Onji M. Serum paraoxonase activity and genotype distribution in Japanese patients with diabetes mellitus. Intern Med. 1998;37:581-584.
[79] Gnasso A, Motti C, Irace C, Di G, I, Pujia A, Leto E, Ciamei M, Crivaro A, Bernardini S, Federici G, Cortese C. The Arg allele in position 192 of PON1 is associated with carotid atherosclerosis in subjects with elevated HDLs. Atherosclerosis. 2002;164:289-295.
[80] Zuliani G, Cherubini A, Volpato S, Palmieri E, Mecocci P, De Rango P, Cao P, Costantini F, Mezzetti A, Mascoli F, Senin U, Fellin R. Genetic factors associated with the absence of atherosclerosis in octogenarians. J Gerontol A Biol Sci Med Sci. 2002;57:M611-M615.
[81] Mackness MI, Arrol S, Mackness B, Durrington PN. The alloenzymes of paraoxonase determine the effectiveness of high-density lipoprotein in protecting low density lipoprotein against lipid-peroxidation. Lancet. 1997;349:851- 852.
[82] Aviram M, Hardk E, Vaya J, Mahmood S, Milo S, Hoffman A, Billicke S, Draganov D, Rosenblat M: Human serum paraoxonase (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid arteriosclerotic lesions. Circulation. 2000; 101: 2510-2517.
[83] Ranade K, Kirchgessner T.G, Iakoubova O.A, Devlin J.J, Delmonte T, Vishnupad P and at al. Evaluation of the paraoxonases as candidate genes for stroke: Gln192Arg polymorphism 1 gene is associated with increased risk of stroke. Strock. 2005;36:2346-2350.
[84] Ozkok E, Aydin M, Babalik E, Ozbek Z, Ince N, Kara I. Combined impact of matrix metalloproteinase-3 andparaoxonase 1 55/192 gene variants on coronaryartery disease in Turkish patients. Med Sci Monit. 2008; 14(10): 536-542.
[85] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in determining normal plasma lipid and lipoprotein variation. Am J Hum Genet 1985;37:265-8.
[86] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis 1988;8:1-21.
[87] Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group, Hixson JE. Apolipoprotein E polymorphisms affect atherosclerosis in young males. Arterioscler Thromb 1991;11:1237-44.
[88] Luo CC, Li WH, Moore MN, et al. Structure and evolution of the apolipoprotein multigene family. J Mol Biol 1986;187:325-40.
[89] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis 1988;8:1-21.
[90] Weintraub MS, Eisenberg S, Breslow JL. Dietary fat clearance in normal subjects is regulated by genetic variation in apolipoprotein E. J Clin Invest 1987;80:1571-7.
[91] Hanis CL, Hewett-Emmett D, Douglas TC, et al. Effects of the apolipoprotein E polymorphism on levels of lipids, lipoproteins, and apolipoproteins among Mexican-Americans in Starr County, Texas. Arterioscler Thromb 1991;11:362-70.
[92] Kataoka S, Robbins DC, Cowan LD, et al. Apolipoprotein E polymorphism in American Indians and its relation to plasma lipoproteins and diabetes: the Strong Heart Study. Arterioscler Thromb Vasc Biol 1996;16:918-25.
[93] Schaefer EJ, Lamon-Fava S, Johnson S, et al. Effects of gender and menopausal status on the association of apolipoprotein E phenotype with plasma lipoprotein levels: results from the Framingham Offspring Study. Arterioscler Thromb Vasc Biol 1994;14:1105-13.
[94] Hallman DM, Boerwinkle E, Saha N, et al. The apolipoprotein E polymorphism: a comparison of allele frequencies and effects in nine populations. Am J Hum Genet 1991;49:338-49.
[95] Lehtinen S, Lehtimaki T, Sisto T, et al. Apolipoprotein E polymorphism, serum lipids, myocardial infarction and severity of angiography verified coronary artery disease in men and women. Atherosclerosis 1995;114:83-91.
[96] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in determining normal plasma lipid and lipoprotein variation. Am J Hum Genet 1985;37:268-85.
[97] Ventakaramana P, Chengal RE and Ferrell RE. Apolipoprotein E polymorphism in two populations of Andru Pradesh. Ind J Hum Genet 2002; 3: 1 5.
[98] Fallah S, Seifi M, Firoozrai M, Godarzi T, Jafarzadeh M, Ghohari L.H. Influence of apo E gene polymorphism on Coronary artery disease. Proceedings of the International Coference on Cellular and Molecular Bioengineering; 2009 sept 23-25; Amsterdam, The Netherlands, 2009
[99] Uterman G, Hardewing A and Zimmer F. Apolipoprotein E phenotypes in patients with myocardial infarction. Hum Genet. 1984; 65: 237-241.
[100] Lehtinens Lehtimalci T, Sisto, Salenius TP, Mikkila M and Jakela H. Apolipoprotein E polymorphism, serum lipid, myocardial infarction and severity of angiographically verified coronary datery disease in men and women . Atheroscelorosis; 1995; 114: 83-91.
[101] Dembinska Kiee A, Kawecka- Jaszez K, Kwasniak M, Gaevaro I, Pankiewicz J and Maiczewsiea Maleec M. Apo E isoforms , insulin out put and plasma lipid levels in essential by hypertension . Eur J Clin Invest, 1998; 28: 95-99.
[102] Yilmas H, Isbir J, Agachan B and Aydin M. Is epsilon 4 allele of apolipoprotein E associated with more severe end stage in essential hypertension? Cell Biochem . Funct 2001; 19: 191-195.
[103] Li X, Duy, DUY and Huang X. Association of apolipoprotein E gene polymorphism with essential hypertension and its complication. Clin Exp Med. 2003; 2: 175-179.
[104] Couderc R, Mahleumof, Bailleu S, Fencon G, Mary R, Fermahken J. Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. Stroke 1993; 24: 661-664.
[105] Sealey, J.E., James, G.D., Laragh, J.H., 1995. The renin-angiotensin- aldosterone system for normal regulation of blood pressure and sodium and potassium homeostasis. In: Laragh, J.H., Brenner, B.M._Eds.., Hypertension. Pathophysiology, Diagnosis and Management, vol. 2, Raven Press, New York, NY, USA, pp. 1763-1796
[106] Hall, J.H., Mizelle, H.L., Woods, L.L., 1986. The renin-angiotensin system and long-term regulation of blood pressure. J. Hypertens. 4, 387- 397.
[107] Dzau, V.J., 1993. Tissue renin-angiotensin system in myocardial hypertrophy and failure. Arch. Intern. Med. 153, 937-942.
[108] Campbell, D.J., 1987. Tissue renin-angiotensin system: sites of angiotensin formation. J. Cardiovasc. Pharmacol. 10_Suppl. 7., S1-S8.
[109] Urata, H., Nishimura, H., Ganten, D., 1996. Chymase-dependent angiotensin II forming system in humans. Am. J. Hypertens. 9, 277-277.
[110] MacKay, J.H., Arcuri, K.E., Goldberg, A.I., Snapinn, S.M., Sweet, C.S., 1996. Losartan and low-dose hydrochlorothiazide in patients with essential hypertension. A double-blind placebo-controlled trial of concomitant administration compared with individual components. Arch. Intern. Med. 156, 278-285.
[111] Azizi, M., Guyene, T.T., Chatellier, G., Wargon, M., Me'nard, J., 1997. Additive effects of losartan and enalapril on blood pressure and plasma active renin. Hypertension 29, 634-640.
[112] Sharpe, N., Murphy, J., Smith, H., Hannon, S., 1988. Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction. Lancet i, 255-259.
[113] Sharpe, N., Smith, H., Murphy, J., Greaves, S., Hart, H., Gamble, G., 1991. Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition. Lancet 337, 872-876.
[114] Pfeffer, M.A., Braunwald, E., Moye', L.A., Basta, L., Brown, E.J. Jr., Cuddy, T.E., Davis, B.R., Geltman, E.M., Goldman, S., Flaker, G.C., Klein, M., Lamas, G.A., Packer, M., Rouleau, J., Rouleau, J.L., Rutherford, J., Wertheimer, J.H., Hawkins, C.M., 1992. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N. Engl. J. Med. 327, 669-677, on behalf of the SAVE Investigators.
[115] ACE Inhibitor Myocardial Infarction Collaborative Group, 1998. Indications for ACE inhibitors in the early treatment of acute myocardial infarction. Systematic overview of individual data from 100,000 patients in randomized trials. Circulation 97, 2202-2212.