Search

In the morning a healthy 40 years old female had a successful spinal anesthetic with bupivacaine 1% 10 mg for hemorrhoidectomy followed by a second injection at midnight for severe pain. The second traumatic injection caused a conus medullaris/cauda equina lesion discovered by MRI 45 days later. The contribution of hyperbaric bupivacaine dosage and pencil point needle is discussed.

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., {"references":["Maton, Anthea, Roshan L,et al. Human Biology and Health. Englewood\nCliffs, New Jersey, USA: Prentice Hall. (1993); ISBN 0-13-981176-1.\nOCLC 32308337","Ridker PM. Inflammation, atherosclerosis, and cardiovascular risk: an\nepidemiologic view. Blood Coagul Fibrinolysis. 1999;10(suppl 1):S9-\nS12.","Crouse JR, Grobbee DE, O-Leary DH, et al. Measuring effects on intima\nmedia thickness: an evaluation of rosuvastatin in subclinical\natherosclerosisÔÇöthe rationale and methodology of the METEOR study.\nCardiovasc Drugs Ther. 2004;18:231-238.","Viles-Gonzalez JF, Fuster V, Badimon JJ. Atherothrombosis: a\nwidespread disease with unpredictable and life-threatening\nconsequences. Eur Heart J. 2004;25: 1197-1207.","Jensen LO,Thayssen P, Pedersen KE, et al. Regression of coronary\natherosclerosis by simvastatin: a serial intravascular ultrasound study.\nCirculation. 2004;110: 265-270.","Rauch U, Osende JI, Fuster V, et al. Thrombus formation on\natherosclerotic plaques: pathogenesis and clinical consequences. Ann\nIntern Med. 2001;134:224-238.","Ohashi R, Mu H,Yao Q, et al. Atherosclerosis: immunopathogenesis and\nimmunotherapy. Med Sci Monit. 2004; 10:RA255-RA260.","Hansson GK. Inflammation, atherosclerosis, and coronary artery disease.\nN Engl J Med. 2005;352: 1685-1695.","Ben-Haim S, Israel O. PET/CT for atherosclerotic plaque imaging. QJ\nNucl Med Mol Imaging. 2006;50: 53-60.\n[10] Van Mieghem CAG, McFadden EP, de Feyter PJ, et al. Noninvasive\ndetection of subclinical coronary atherosclerosis coupled with\nassessment of changes in plaque characteristics using novel invasive\nimaging modalities. The Integrated Biomarker and Imaging Study. J Am\nColl Cardiol. 2006;47:1134-1142.\n[11] Weissberg PL. Atherogenesis: current understanding of the causes of\natheroma. Heart. 2000;83:247-252.\n[12] Carlos TM , Harlan JM. Leukocyte-endothelial adhesion molecules.\nBlood 1994;84:2068-101.\n[13] Vora DK, Fang ZT, Liva SM, et al. Induction of P-selectin by oxidized\nlipoproteins. Separate effects on synthesis and surface expression. Circ\nRes 1997;80:810-8.\n[14] Iiyama K, Hajra L, Iiyama M, et al. Patterns of vascular cell adhesion\nmolecule-1 and intercellular adhesion molecule-1 expression in rabbit\nand mouse atherosclerotic lesions and at sites predisposed to lesion\nformation. Circ Res 1999;85:199-207.\n[15] Gu L, Okada Y, Clinton SK, et al. Absence of monocyte chemoattractant\nprotein-1 reduces atherosclerosis in low density lipoprotein receptordeficient\nmice. Mol Cell 1998;2:275-81.\n[16] Watson AD, Leitinger N, Navab M, et al. Structural identification by\nmass spectrometry of oxidized phospholipids in minimally oxidized low\ndensity lipoprotein that induce monocyte/endothelial interactions and\nevidence for their presence in vivo. J Biol Chem 1997;272:13597-607.\n[17] von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and\narteriosclerosis. Role of cholesterol efflux and reverse cholesterol\ntransport. Arterioscler Thromb Vasc Biol 2001; 21:13-27.\n[18] Libby P, Warner SJ, Salomon RN, et al. Production of platelet-derived\ngrowth factor-like mitogen by smooth-muscle cells from human\natheroma. N Engl J Med 1988;318:1493-8.\n[19] Higashiyama S, Abraham JA, Miller J, et al. A heparin-binding growth\nfactor secreted by macrophage-like cells that is related to EGF. Science\n1991;251:936-9.\n[20] Libby P. Changing concepts of atherogenesis. J Intern Med 2000;\n247:349-58\n[21] Amento EP, Ehsani N, Palmer H, et al. Cytokines and growth factors\npositively and negatively regulate interstitial collagen gene expression in\nhuman vascular smooth muscle cells. Arterioscler Thromb\n1991;11:1223-30\n[22] van der Wal AC, Becker AE, van der Loos CM, et al. Site of intimal\nrupture or erosion of thrombosed coronary atherosclerotic plaques is\ncharacterized by an inflammatory process irrespective of the dominant\nplaque morphology. Circulation 1994;89:36-44.\n[23] Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix\nmetalloproteinases and matrix degrading activity in vulnerable regions\nof human atherosclerotic plaques. J Clin Invest 1994;94:2493-503.\n[24] Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s.\nNature 1993;362:801- 9.\n[25] Libby P. Molecular bases of the acute coronary syndromes. Circulation\n1995;91:2844- 50.\n[26] Davies MJ. Stability and instability: two faces of coronary\natherosclerosis. The Paul Dudley White Lecture 1995. Circulation 1996;\n94:2013-20.\n[27] Hangartner JR, Charleston AJ, Davies MJ, Thomas AC. Morphological\ncharacteristics of clinically significant coronary artery stenosis in stable\nangina. Br Heart J 1986;56:501-8.\n[28] Blankenhorn DH, Hodis HN (August 1993). \"Atherosclerosis--reversal\nwith therapy\". The Western journal of medicine 159 (2): 172-9. PMID\n8212682.\n[29] Botto N, Rizza A, Colombo M, Mazzone A, Manfredi S, Masetti S, et al.\nEvidence for DNA damage in patients with coronary artery disease.\nMutat Res 2001;493:23- 30.\n[30] Andreassi MG, Botto N, Cocci F, et al. Methylenetetrahydrofolate\nreductase gene C677T polymorphism, homocysteine, vitamin B12, and\nDNA damage in coronary artery disease. Hum Genet 2003;112:171-7.\n[31] Botto N, Berti S, Manfredi S, et al. Detection of mtDNA with 4977bp\ndeletion in blood cells and atherosclerotic lesions of patients with\ncoronary artery disease. Mutat Res 2005;570:81- 8.\n[32] Henney AM, Wakeley PR, Davies MJ, et al. Localization of stromelysin\ngene expression in atherosclerotic plaques by in situ hybridization. Proc\nNatl Acad Sci USA 1991;88:8154_/8.\n[33] Galis, Z.S., Khatri, J.J., 2002. Matrix metalloproteinases in vascular\nremodeling and atherogenesis: the good, the bad, and the ugly. Circ. Res.\n90 (3), 251-262.\n[34] Newby, A.C., 2005. Dual role of matrix metalloproteinases (matrixins)\nin intimal thickening and atherosclerotic plaque rupture. Physiol Rev. 85\n(1), 1-31.\n[35] Newby, A.C., Johnson, J.L., 2005. Genetic strategies to elucidate the\nroles of matrix metalloproteinases in atherosclerotic plaque growth and\nstability. Circ. Res. 97 (10), 958-960.\n[36] Hayashidani, S., Tsutsui, H., Ikeuchi, M., et al. Targeted deletion of\nMMP 2 attenuates early LV rupture and late remodeling after\nexperimental myocardial infarction.2003; Am. J. Physiol. Heart Circ.\nPhysiol. 285 (3), H1229-H1235\n[37] Heymans, S., Luttun, A., Nuyens, D., et al. Inhibition of plasminogen\nactivators or matrix metalloproteinases prevents cardiac rupture but\nimpairs therapeutic angiogenesis and causes cardiac failure. 1999;\nNature Med. 5 (10), 1135-1142.\n[38] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S.,\nOkada, Y., Targeted deletion or pharmacological inhibition of MMP-2\nprevents cardiac rupture after myocardial infarction in mice. 2005a; J.\nClin. Invest. 115 (3), 599-609.\n[39] Matsumura, S., Iwanaga, S., Mochizuki, S., Okamoto, H., Ogawa, S.,\nOkada, Y.,. Targeted deletion or pharmacological inhibition of MMP-2\nprevents cardiac rupture after myocardial infarction in mice. 2005b; J.\nClin. Invest. 115 (3), 599-609.\n[40] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection\nfrom ischemia/reperfusion injury by targeted deletion of matrix\nmetalloproteinase-9. 2002a; Cardiovasc. Res. 54 (3), 549-558.\n[41] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection\nfrom ischemia/reperfusion injury by targeted deletion of matrix\nmetalloproteinase-9.2002b; Cardiovasc. Res. 54 (3), 549-558.\n[42] Romanic, A.M., Harrison, S.M., Bao, W., et al. Myocardial protection\nfrom ischemia/reperfusion injury by targeted deletion of matrix\nmetalloproteinase-9.2002c; Cardiovasc. Res. 54 (3), 549-558.\n[43] Deschamps, A.M., Yarbrough, W.M., Squires, C.E., et al. Trafficking of\nthe membrane type-1 matrix metalloproteinase in ischemia and\nreperfusion: relation to interstitial membrane type-1 matrix\nmetalloproteinase activity. 2005; Circulation 111 (9), 1166-1174.\n[44] Fedak, P.W., Smookler, D.S., Kassiri, Z., et al. TIMP-3 deficiency leads\nto dilated cardiomyopathy.2004; Circulation 110 (16), 2401-2409.\n[45] Longo, G.M., Xiong, W., Greiner, T.C., Zhao, Y., Fiotti, N., Baxter,\nB.T.,. Matrix metalloproteinases 2 and 9 work in concert to produce\naortic aneurysms. 2002; J. Clin. Invest. 110 (5), 625-632.\n[46] Johnson, J.L., George, S.J., Newby, A.C., Jackson, C.L.,. Divergent\neffects of matrix metalloproteinases 3, 7, 9, and 12 on atherosclerotic\nplaque stability in mouse brachiocephalic arteries. 2005; Proc. Natl.\nAcad. Sci. USA 102 (43), 15575-15580.\n[47] Chase, A.J., Newby, A.C.,. Regulation of matrix metalloproteinase\n(matrixin) genes in blood vessels: a multi-step recruitment model for\npathological remodelling. 2003; J. Vasc. Res. 40 (4), 329-343.\n[48] Ye S, Watts GF, Mandalia S, Humphries SE, Henney AM. Preliminary\nreport: genetic variation in the human stromelysin promoter is associated\nwith progression of coronary atherosclerosis. Br Heart J 1995;73:209-\n15.\n[49] Ye S, Eriksson P, Hamsten A, Kurkinen M, Humphries SE, Henney AM.\nProgression of coronary atherosclerosis is associated with a common\ngenetic variant of the human stromelysin-1 promoter which results in\nreduced gene expression. J Biol Chem 1996;271:13055-60.\n[50] Humphries S, Bauters C, Meirhaeghe A, Luong L, Bertrand M, Amouyel\nP. The 5A6A polymorphism in the promoter of the stromelysin-1\n(MMP3) gene as a risk factor for restenosis. Eur Heart J 2002;23:721-5.\n[51] Seifi M, Fallah S, Firoozrai M. Influence of Genetic Polymorphism in\nMatrix Metalloproteinase-3 on Extent of Coronary Atherosclerosis and\nRisk of Coronary Artery Stenosis. Archives Medical Research. In press\n[52] Primo-Parmo SL, Sorenson RC, Teiber J, La Du BN. The human serum\nparaoxonase/arylesterase gene (PON1) is one member of a multigene\nfamily. Genomics. 1996;33:498 -507.\n[53] Watson AD, Berliner JA, Hama SY, La Du BN, Faull KF, Fogelman\nAM, Navab M. Protective effect of high density lipoprotein associated\nparaoxonase. Inhibition of the biological activity of minimally oxidized\nlow density lipoprotein. J Clin Invest. 1995;96:2882-2891.\n[54] Ng CJ, Wadleigh DJ, Gangopadhyay A, Hama S, Grijalva VR, Navab\nM, Fogelman AM, Reddy ST. Paraoxonase-2 is a ubiquitously expressed\nprotein with antioxidant properties and is capable of preventing\ncellmediated oxidative modification of low density lipoprotein. J Biol\nChem. 2001;276:44444-44449.\n[55] Li B, Sedlacek M, Manoharan I, Boopathy R, Duysen EG, Masson P,\nLockridge O: Butyrylcholinesterase, paraoxonase, and albumin esterase,\nbut not carboxylesterase, are present in human Plasma. Biochem\nPharmacol. 2005;70: 1673-1684.\n[56] Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La\nDu BN. Paraoxonase inhibits high-density lipoprotein oxidation and\npreserves its functions: a possible peroxidative role for praoxonase. J\nClin Invest. 1998;101:1581-1590.\n[57] Durrington P.N, Mackness B and Mackness M.I. Parooxonase and\natherosclerosis. Arterioscler.Tromb.Vasc.Biol.2001;21:473-480\n[58] Kuremoto K, Watanabe Y, Ohmura H et al: R/R genotype of human\nparaoxonase (PON1) is more protective against lipoprotein oxidation\nand coronary artery disease in Japanese subjects. J Atheroscler Thromb,\n2003; 10: 85-92\n[59] Huang Y, Mironova M, Lopes-Virella MF: Oxidized LDL stimulates\nmatrix metalloproteinase-1 expression in human vascular endothelial\ncells. Arterioscler Thromb Vasc Biol, 1999; 19: 2640-47\n[60] Navab M, Berliner JA, Watson AD et al: The yin and yang of oxidation\nin the development of fatty streak: a review based on the 1994 George\nLyman Duff Memorial Lecture. Arterioscler Thromb Vasc Biol, 1996;\n16: 831-42\n[61] Navab M, Hama SY, Anantharamaiah GM et al: Normal high-density\nlipoprotein inhibits three steps in the formation of mildly oxidized low\ndensity lipoprotein: steps 2 and 3. J Lipid Res, 2000; 41: 1495-508\n[62] Mackness MI, Durrington PN: HDL, its enzymes and its potential to infl\nuence lipid peroxidation. Atherosclerosis, 1995; 115: 243-53\n[63] Watson AD, Berliner JA, Hama SY et al: Protective effect of high\ndensity lipoprotein associated paraoxonase: inhibition of biological\nactivity of minimally oxidized low density lipoprotein. J Clin Invest,\n1995; 96: 2882-91\n[64] Blatter MC, James RW, Messmer S et al: Identifi cation of a distinct\nhuman high-density lipoprotein subspecies defi ned by a lipoproteinassociated\nprotein, K-45: identity of K-45 with paraoxonase. Eur J\nBiochem, 1993; 211: 871-79\n[65] Kelso GJ, Stuart WD, Richter RJ et al: Apolipoprotein J is associated\nwith paraoxonase in human plasma. Biochemistry, 1994; 33: 832-39\n[66] Humbert R, Adler DA, Disteche CM et al: The molecular basis of the\nhuman serum paraoxonase activity polymorphism. Nat Genet, 1993; 3:\n73-76\n[67] Adkins S, Gan KN, Mody M, La du DN: Molecular basis for the\npolymorphic form of human serum paraoxoanase/arylesterase: glutamine\nor arginine at position 191, for the respective A or B allozymes. Am J\nHum Genet, 1993; 52: 598-60\n[68] Fortunato G, Rubba P, Panico S, Trono D, Tinto N, Mazzaccara C, De\nMichele M, Iannuzzi A, Vitale DF, Salvatore F, Sacchetti L. A\nparaoxonase gene polymorphism, PON 1 (55), as an independent risk\nfactor for increased carotid intima-media thickness in middle-aged\nwomen. Atherosclerosis. 2003;167:141-148.\n[69] Markus H, Kapozsta Z, Ditrich R, Wolfe C, Ali N, Powell J, Mendell M,\nCullinane M. Increased common carotid intima-media thickness in UK\nAfrican Caribbeans and its relation to chronic inflammation and vascular\ncandidate gene polymorphisms. Stroke. 2001;32:2465-2471.\n[70] Jarvik GP, Hatsukami TS, Carlson C, Richter RJ, Jampsa R, Brophy VH,\nMargolin S, Rieder M, Nickerson D, Schellenberg GD, Heagerty PJ,\nFurlong CE. Paraoxonase activity, but not haplotype utilizing the linkage\ndisequilibrium structure, predicts vascular disease. Arterioscler Thromb\nVasc Biol. 2003;1923:1465-1471\n[71] Pallaud C, Sass C, Zannad F, Siest G, Visvikis S. APOC3, CETP,\nfibrinogen, and MTHFR are genetic determinants of carotid intimamedia\nthickness in healthy men (the Stanislas cohort). Clin Genet.\n2001;59:316-324.\n[72] Schmidt H, Schmidt R, Niederkorn K, Gradert A, Schumacher M,\nWatzinger N, Hartung HP, Kostner GM. Paraoxonase PON1\npolymorphism leu-Met54 is associated with carotid atherosclerosis:\nresults of the Austrian Stroke Prevention Study. Stroke. 1998;29:2043-\n2048.\n[73] Koch M, Hering S, Barth C, Ehren M, Enderle MD, Pfohl M.\nParaoxonase1 192 Gln/Arg gene polymorphism and cerebrovascular\ndisease: interaction with type 2 diabetes. Exp Clin Endocrinol Diabetes.\n2001;109:141-145.\n[74] Cao H, Girard-Globa A, Serusclat A, Bernard S, Bondon P, Picard S,\nBerthezene F, Moulin P. Lack of association between carotid intimamedia thickness and paraoxonase gene polymorphism in noninsulin\ndependent diabetes mellitus. Atherosclerosis. 1998;138: 361-366.\n[75] Dessi M, Gnasso A, Motti C, Pujia A, Irace C, Casciani S, Staffa F,\nFederici G, Cortese C. Influence of the human paraoxonase\npolymorphism (PON1 192) on the carotid-wall thickening in a healthy\npopulation. Coron Artery Dis. 1999;10:595-599.\n[76] Jarvik GP, Rozek LS, Brophy VH, Hatsukami TS, Richter RJ,\nSchellenberg GD, Furlong CE. Paraoxonase (PON1) phenotype is a\nbetter predictor of vascular disease than is PON1(192) or PON1(55)\ngenotype. Arterioscler Thromb Vasc Biol. 2000;20:2441-2447.\n[77] Leus FR, Wittekoek ME, Prins J, Kastelein JJ, Voorbij HA. Paraoxonase\ngene polymorphisms are associated with carotid arterial wall thickness in\nsubjects with familial hypercholesterolemia. Atherosclerosis. 2000;\n149:371-377.\n[78] Sakai T, Matsuura B, Onji M. Serum paraoxonase activity and genotype\ndistribution in Japanese patients with diabetes mellitus. Intern Med.\n1998;37:581-584.\n[79] Gnasso A, Motti C, Irace C, Di G, I, Pujia A, Leto E, Ciamei M, Crivaro\nA, Bernardini S, Federici G, Cortese C. The Arg allele in position 192 of\nPON1 is associated with carotid atherosclerosis in subjects with elevated\nHDLs. Atherosclerosis. 2002;164:289-295.\n[80] Zuliani G, Cherubini A, Volpato S, Palmieri E, Mecocci P, De Rango P,\nCao P, Costantini F, Mezzetti A, Mascoli F, Senin U, Fellin R. Genetic\nfactors associated with the absence of atherosclerosis in octogenarians. J\nGerontol A Biol Sci Med Sci. 2002;57:M611-M615.\n[81] Mackness MI, Arrol S, Mackness B, Durrington PN. The alloenzymes of\nparaoxonase determine the effectiveness of high-density lipoprotein in\nprotecting low density lipoprotein against lipid-peroxidation. Lancet.\n1997;349:851- 852.\n[82] Aviram M, Hardk E, Vaya J, Mahmood S, Milo S, Hoffman A, Billicke\nS, Draganov D, Rosenblat M: Human serum paraoxonase (PON1) Q and\nR selectively decrease lipid peroxides in human coronary and carotid\narteriosclerotic lesions. Circulation. 2000; 101: 2510-2517.\n[83] Ranade K, Kirchgessner T.G, Iakoubova O.A, Devlin J.J, Delmonte T,\nVishnupad P and at al. Evaluation of the paraoxonases as candidate\ngenes for stroke: Gln192Arg polymorphism 1 gene is associated with\nincreased risk of stroke. Strock. 2005;36:2346-2350.\n[84] Ozkok E, Aydin M, Babalik E, Ozbek Z, Ince N, Kara I. Combined\nimpact of matrix metalloproteinase-3 andparaoxonase 1 55/192 gene\nvariants on coronaryartery disease in Turkish patients. Med Sci Monit.\n2008; 14(10): 536-542.\n[85] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in\ndetermining normal plasma lipid and lipoprotein variation. Am J Hum\nGenet 1985;37:265-8.\n[86] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and\natherosclerosis. Arteriosclerosis 1988;8:1-21.\n[87] Pathobiological Determinants of Atherosclerosis in Youth (PDAY)\nResearch Group, Hixson JE. Apolipoprotein E polymorphisms affect\natherosclerosis in young males. Arterioscler Thromb 1991;11:1237-44.\n[88] Luo CC, Li WH, Moore MN, et al. Structure and evolution of the\napolipoprotein multigene family. J Mol Biol 1986;187:325-40.\n[89] Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and\natherosclerosis. Arteriosclerosis 1988;8:1-21.\n[90] Weintraub MS, Eisenberg S, Breslow JL. Dietary fat clearance in normal\nsubjects is regulated by genetic variation in apolipoprotein E. J Clin\nInvest 1987;80:1571-7.\n[91] Hanis CL, Hewett-Emmett D, Douglas TC, et al. Effects of the\napolipoprotein E polymorphism on levels of lipids, lipoproteins, and\napolipoproteins among Mexican-Americans in Starr County, Texas.\nArterioscler Thromb 1991;11:362-70.\n[92] Kataoka S, Robbins DC, Cowan LD, et al. Apolipoprotein E\npolymorphism in American Indians and its relation to plasma\nlipoproteins and diabetes: the Strong Heart Study. Arterioscler Thromb\nVasc Biol 1996;16:918-25.\n[93] Schaefer EJ, Lamon-Fava S, Johnson S, et al. Effects of gender and\nmenopausal status on the association of apolipoprotein E phenotype with\nplasma lipoprotein levels: results from the Framingham Offspring Study.\nArterioscler Thromb Vasc Biol 1994;14:1105-13.\n[94] Hallman DM, Boerwinkle E, Saha N, et al. The apolipoprotein E\npolymorphism: a comparison of allele frequencies and effects in nine\npopulations. Am J Hum Genet 1991;49:338-49.\n[95] Lehtinen S, Lehtimaki T, Sisto T, et al. Apolipoprotein E polymorphism,\nserum lipids, myocardial infarction and severity of angiography verified\ncoronary artery disease in men and women. Atherosclerosis\n1995;114:83-91.\n[96] Sing CF, Davignon J. Role of the apolipoprotein E polymorphism in\ndetermining normal plasma lipid and lipoprotein variation. Am J Hum\nGenet 1985;37:268-85.\n[97] Ventakaramana P, Chengal RE and Ferrell RE. Apolipoprotein E\npolymorphism in two populations of Andru Pradesh. Ind J Hum Genet\n2002; 3: 1 5.\n[98] Fallah S, Seifi M, Firoozrai M, Godarzi T, Jafarzadeh M, Ghohari L.H.\nInfluence of apo E gene polymorphism on Coronary artery disease.\nProceedings of the International Coference on Cellular and Molecular\nBioengineering; 2009 sept 23-25; Amsterdam, The Netherlands, 2009\n[99] Uterman G, Hardewing A and Zimmer F. Apolipoprotein E phenotypes\nin patients with myocardial infarction. Hum Genet. 1984; 65: 237-241.\n[100] Lehtinens Lehtimalci T, Sisto, Salenius TP, Mikkila M and Jakela H.\nApolipoprotein E polymorphism, serum lipid, myocardial infarction and\nseverity of angiographically verified coronary datery disease in men and\nwomen . Atheroscelorosis; 1995; 114: 83-91.\n[101] Dembinska Kiee A, Kawecka- Jaszez K, Kwasniak M, Gaevaro I,\nPankiewicz J and Maiczewsiea Maleec M. Apo E isoforms , insulin out\nput and plasma lipid levels in essential by hypertension . Eur J Clin\nInvest, 1998; 28: 95-99.\n[102] Yilmas H, Isbir J, Agachan B and Aydin M. Is epsilon 4 allele of\napolipoprotein E associated with more severe end stage in essential\nhypertension? Cell Biochem . Funct 2001; 19: 191-195.\n[103] Li X, Duy, DUY and Huang X. Association of apolipoprotein E gene\npolymorphism with essential hypertension and its complication. Clin\nExp Med. 2003; 2: 175-179.\n[104] Couderc R, Mahleumof, Bailleu S, Fencon G, Mary R, Fermahken J.\nPrevalence of apolipoprotein E phenotypes in ischemic cerebrovascular\ndisease. Stroke 1993; 24: 661-664.\n[105] Sealey, J.E., James, G.D., Laragh, J.H., 1995. The renin-angiotensin-\naldosterone system for normal regulation of blood pressure and sodium\nand potassium homeostasis. In: Laragh, J.H., Brenner, B.M._Eds..,\nHypertension. Pathophysiology, Diagnosis and Management, vol. 2,\nRaven Press, New York, NY, USA, pp. 1763-1796\n[106] Hall, J.H., Mizelle, H.L., Woods, L.L., 1986. The renin-angiotensin\nsystem and long-term regulation of blood pressure. J. Hypertens. 4, 387-\n397.\n[107] Dzau, V.J., 1993. Tissue renin-angiotensin system in myocardial\nhypertrophy and failure. Arch. Intern. Med. 153, 937-942.\n[108] Campbell, D.J., 1987. Tissue renin-angiotensin system: sites of angiotensin\nformation. J. Cardiovasc. Pharmacol. 10_Suppl. 7., S1-S8.\n[109] Urata, H., Nishimura, H., Ganten, D., 1996. Chymase-dependent\nangiotensin II forming system in humans. Am. J. Hypertens. 9, 277-277.\n[110] MacKay, J.H., Arcuri, K.E., Goldberg, A.I., Snapinn, S.M., Sweet, C.S.,\n1996. Losartan and low-dose hydrochlorothiazide in patients with\nessential hypertension. A double-blind placebo-controlled trial of\nconcomitant administration compared with individual components. Arch.\nIntern. Med. 156, 278-285.\n[111] Azizi, M., Guyene, T.T., Chatellier, G., Wargon, M., Me'nard, J., 1997.\nAdditive effects of losartan and enalapril on blood pressure and plasma\nactive renin. Hypertension 29, 634-640.\n[112] Sharpe, N., Murphy, J., Smith, H., Hannon, S., 1988. Treatment of\npatients with symptomless left ventricular dysfunction after myocardial\ninfarction. Lancet i, 255-259.\n[113] Sharpe, N., Smith, H., Murphy, J., Greaves, S., Hart, H., Gamble, G.,\n1991. Early prevention of left ventricular dysfunction after myocardial\ninfarction with angiotensin-converting-enzyme inhibition. Lancet 337,\n872-876.\n[114] Pfeffer, M.A., Braunwald, E., Moye', L.A., Basta, L., Brown, E.J. Jr.,\nCuddy, T.E., Davis, B.R., Geltman, E.M., Goldman, S., Flaker, G.C.,\nKlein, M., Lamas, G.A., Packer, M., Rouleau, J., Rouleau, J.L.,\nRutherford, J., Wertheimer, J.H., Hawkins, C.M., 1992. Effect of\ncaptopril on mortality and morbidity in patients with left ventricular\ndysfunction after myocardial infarction. N. Engl. J. Med. 327, 669-677,\non behalf of the SAVE Investigators.\n[115] ACE Inhibitor Myocardial Infarction Collaborative Group, 1998.\nIndications for ACE inhibitors in the early treatment of acute myocardial\ninfarction. Systematic overview of individual data from 100,000 patients\nin randomized trials. Circulation 97, 2202-2212."]}