Genetic markers: Potential candidates for cardiovascular disease

International Journal of Cardiology

Volumn 220, Issue , 2016, Pages 914-923

  Rather, Riyaz Ahmad ^a   Dhawan, Veena ^a  

^a POSTGRADUATE INSTITUTE OF MEDICAL EDUCATION AND RESEARCH   (India)

Author keywords

Biomarker; Cardiovascular disease; Genomics; Proteomics; Single nucleotide polymorphism

Indexed keywords

5,10 METHYLENETETRAHYDROFOLATE REDUCTASE (FADH2); BIOLOGICAL MARKER; CHOLESTEROL ESTER TRANSFER PROTEIN; DIPEPTIDYL CARBOXYPEPTIDASE; ESTROGEN RECEPTOR; GLYCOPROTEIN IIIA; LIPOPROTEIN A; GENETIC MARKER; MESSENGER RNA;

BIOINFORMATICS; CARDIOVASCULAR DISEASE; CARDIOVASCULAR RISK; DNA POLYMORPHISM; FIBRINOLYSIS; GENE EXPRESSION; GENETIC MARKER; GENOMICS; HUMAN; IMAGING; METABOLOMICS; NONHUMAN; PRIORITY JOURNAL; PROTEOMICS; REVIEW; THROMBOSIS; GENETIC ASSOCIATION STUDY; GENETICS; METABOLISM; RISK FACTOR; TRENDS;

BIOMARKERS; CARDIOVASCULAR DISEASES; GENETIC ASSOCIATION STUDIES; GENETIC MARKERS; HUMANS; METABOLOMICS; RISK FACTORS; RNA, MESSENGER;

EID: 84978036911     PISSN: 01675273     EISSN: 18741754     Source Type: Journal    
DOI: 10.1016/j.ijcard.2016.06.251     Document Type: Review

References (186)

1. [1] Braunwald, E.S., Cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities. N. Engl. J. Med. 337:19 (1997), 1360–1369.
2. [2] Raitakari, O.T., Juonala, M., Kahonen, M., et al. Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA 290:17 (2003), 2277–2283.
3. [3] Jokhadar, M., Jacobsen, S.J., Reeder, G.S., Weston, S.A., Roger, V.L., et al. Sudden death and recurrent ischemic events after myocardial infarction in the community. Am. J. Epidemiol. 159:11 (2004), 1040–1046.
4. [4] Panju, A.A., Hemmelgarn, B.R., Guyatt, G.H., Simel, D.L., Is this patient having a myocardial infarction?. JAMA 280:14 (1998), 1256–1263.
5. [5] Pope, J.H., Aufderheide, T.P., Ruthazer, R., et al. Missed diagnoses of acute cardiac ischemia in the emergency department. N. Engl. J. Med. 342:16 (2000), 1163–1170.
6. [6] Naghavi, M., Libby, P., Falk, E., Casscells, S.W., et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: part II. Circulation 108:15 (2003), 1772–1778.
7. [7] Gary, H.G., Choong, C.L., Mark, O., et al. Genetic markers: progress and potential for cardiovascular disease. Circulation 109:25 suppl. 1 (2004), IV47–IV58.
8. [8] Lusis, A.J., Fogelman, A.M., Fomarow, G.C., Genetic basis of atherosclerosis. Part I: new genes and pathways. Circulation 100:13 (2004), 1868–1873.
9. [9] Mc Carthy, J.J., Parker, A., Salem, R., et al. Large scale association analysis for identification of genes underlying premature coronary heart disease: cumulative perspective from analysis of 111 candidate genes. J. Med. Genet. 41:5 (2004), 334–341.
10. [10] Frank, R., Hargreaves, R., Clinical biomarkers in drug discovery and development. Nat. Rev. Drug Discov. 2:7 (2003), 566–580.
11. [11] Petricoin, E.F., Liotta, L.A., Proteomic analysis at the bedside: early detection of cancer. Trends Biotechnol. 20:12 Suppl. (2002), S30–S34.
12. [12] Pepe, M.S., Etzioni, R., Feng, Z., et al. Phases of biomarker development for early detection of cancer. J. Natl. Cancer Inst. 93:14 (2001), 1054–1061.
13. [13] Redberg, R.F., Vogel, R.A., Criqui, M.H., Herrington, D.M., Lima, J.A., Roman, M.J., 34th Bethesda Conference: task force #3–what is the spectrum of current and emerging techniques for the noninvasive measurement of atherosclerosis?. J. Am. Coll. Cardiol. 41:11 (2003), 1886–1898.
14. [14] Manolio, T., Novel risk markers and clinical practice. N. Engl. J. Med. 349:17 (2003), 1587–1589.
15. [15] Ashley, E.A., Hershberger, R.E., Caleshu, C., et al. American Heart Association Advocacy Coordinating Committee. Genetics and cardiovascular disease: a policy statement from the American Heart Association. Circulation 126:1 (2012), 142–157.
16. [16] Guttmacher, A.E., Collins, F.S., Carmona, R.H., The family history–more important than ever. N. Engl. J. Med. 351 (2004), 2333–2336.
17. [17] Lander, E.S., Schork, N.J., Genetic dissection of complex traits. Science 265:5181 (1994), 2037–2048.
18. [18] Risch, N.J., Searching for genetic determinants in the new millennium. Nature 405:6788 (2000), 847–856.
19. [19] Altmuller, J., Palmer, L.J., Fischer, G., Scherb, H., Wjst, M., Genome wide scans of complex human diseases: true linkage is hard to find. Am. J. Hum. Genet. 69:5 (2001), 936–950.
20. [20] Risch, N., Merikangas, K., The future of genetic studies of complex human diseases. Science 273:5281 (1996), 1516–1517.
21. [21] Goodarzi, M.O., Guo, X., Taylor, K.D., et al. Determination and use of haplotypes: ethnic comparison and association of the lipoprotein lipase gene and coronary artery disease in Mexican-Americans. Genet. Med. 5:4 (2003), 322–327.
22. [22] Chakravarti, A., Population genetics: making sense out of sequence. Nat. Genet. 21 (1999), 56–60.
23. [23] Lohmueller, K.E., Pearce, C.L., Pike, M., Lander, E.S., Hirschhorn, J.N., Metaanalysis of genetic association studies supports a contribution of common variants to susceptibility to common disease. Nat. Genet. 33:2 (2003), 177–182.
24. [24] Reich, D.E., Lander, E.S., On the allelic spectrum of human disease. Trends Genet. 17:9 (2001), 502–510.
25. [25] Ramachandran, S.V., Biomarkers of cardiovascular disease, molecular basis and practical considerations. Circulation 113:19 (2006), 2335–2362.
26. [26] Harrap, S.B., Zammit, K.S., Wong, Z.Y.H., et al. Genome wide linkage analysis of the acute coronary syndrome suggests a locus on chromosome 2. Arterioscler. Thromb. Vasc. Biol. 22:5 (2002), 874–878.
27. [27] Hauser, E.R., Granger, C.B., Dowdy, E., et al. A genome wide scan for early-onset coronary artery disease in 438 families: the GENECARD Study. Am. J. Hum. Genet. 75:3 (2004), 436–447.
28. [28] Chiodini, B.D., Barlera, S., Franzosi, M.G., et al. APO B gene polymorphisms and coronary artery disease: a metaanalysis. Atherosclerosis 167:2 (2003), 355–366.
29. [29] Keavney, B., McKenzie, C., Parish, S., et al. For the International Studies of Infarct Survival (ISIS) collaborators, large-scale test of hypothesized associations between the angiotensin-converting-enzyme insertion/deletion polymorphism and myocardial infarction in about 5000 cases and 6000 controls. Lancet 355:9202 (2000), 434–442.
30. [30] Song, Y., Stampfer, M.J., Liu, S., Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Ann. Intern. Med. 141:2 (2004), 137–147.
31. [31] Wang, Q., Advances in the genetic basis of coronary artery disease. Curr. Atheroscler. Rep. 7:3 (2005), 235–241.
32. [32] Cook, S.A., Rosenzweig, A., DNA microarrays: implications for cardiovascular medicine. Circ. Res. 91:7 (2002), 559–564.
33. [33] Napoli, C., Lerman, L.O., Sica, V., Lerman, A., Tajana, G., De Nargis, F., Microarray analysis: a novel research tool for cardiovascular scientists and physicians. Heart 89:6 (2003), 597–604.
34. [34] Danziger, R.S., You, M., Akil, H., Discovering the genetics of complex disorders through integration of genomic mapping and transcriptional profiling. Curr. Hypertens. Rev. 1:1 (2005), 21–34.
35. [35] Hwang, D.M., Dempsey, A.A., Wang, R.X., et al. A genome-based resource for molecular cardiovascular medicine: toward a compendium of cardiovascular genes. Circulation 96:12 (1997), 4146–4203.
36. [36] Barrans, J.D., Allen, P.D., Stamatiou, D., Dzau, V.J., Liew, C.C., Global gene expression profiling of end-stage dilated cardiomyopathy using a human cardiovascular-based cDNA microarray. Am. J. Pathol. 160:6 (2002), 2035–2043.
37. [37] Friddle, C.J., Koga, T., Rubin, E.M., Bristow, J., Expression profiling reveals distinct sets of genes altered during induction and regression of cardiac hypertrophy. Proc. Natl. Acad. Sci. 97:12 (2000), 6745–6750.
38. [38] Sehl, P.D., Tai, J.T.N., Hillan, K.J., et al. Application of cDNA microarrays in determining molecular phenotype in cardiac growth, development, and response to injury. Circulation 101:16 (2000), 1990–1999.
39. [39] Stanton, L.W., Garrard, L.J., Damm, D., et al. Altered patterns of gene expression in response to myocardial infarction. Circ. Res. 86:9 (2000), 939–945.
40. [40] Saiura, A., Kohro, T., Yamamoto, T., et al. Detection of an up-regulation of a group of chemokine genes in murine cardiac allograft in the absence of interferon-gamma by means of DNA microarray. Transplantation 73:9 (2002), 1480–1486.
41. [41] Assmann, G., Cullen, P., Schulte, H., Simple scoring scheme for calculating the risk of acute coronary events based on the 10-year follow-up of the Prospective Cardiovascular Munster (PROCAM) Study. Circulation 105:3 (2002), 310–315.
42. [42] Assmus, B., Urbich, C., Aicher, A., et al. HMG-CoA reductase inhibitors reduce senescence and increase proliferation of endothelial progenitor cells via regulation of cell cycle regulatory genes. Circ. Res. 92:9 (2003), 1049–1055.
43. [43] Ma, J., Liew, C.C., Gene profiling identifies secreted protein transcripts from peripheral blood cells in coronary artery disease. J. Mol. Cell. Cardiol. 35:8 (2003), 993–998.
44. [44] Podgoreanu, M.V., Schwinn, D.A., Genomics and the circulation. Br. J. Anaesthesiol. 93:1 (2004), 140–148.
45. [45] Walsh, G., Jefferis, R., Post-translational modifications in the context of therapeutic proteins. Nat. Biotechnol. 24:10 (2006), 1241–1252.
46. [46] Anderson, L., Candidate-based proteomics in the search for biomarkers of cardiovascular disease. J. Physiol. 563:1 (2005), 23–60.
47. [47] Stanley, B.A., Gundry, R.L., Cotter, R.J., Van Eyk, J.E., Heart disease, clinical proteomics and mass spectrometry. Dis. Markers 20:3 (2004), 167–178.
48. [48] Ping, P., Identification of novel signaling complexes by functional proteomics. Circ. Res. 93:7 (2003), 595–603.
49. [49] Sawicki, G., Jugdutt, B.I., Detection of regional changes in protein levels in the in vivo canine model of acute heart failure following ischemia reperfusion injury: functional proteomics studies. Proteomics 4:7 (2004), 2195–2202.
50. [50] Gramolini, A.O., Kislinger, T., Liu, P.P., MacLennan, D.H., Emili, A., Analyzing the cardiac muscle proteome by liquid chromatography mass spectrometry (LC–MS) based expression proteomics. Methods Mol. Biol. 357 (2007), 15–32.
51. [51] Staniloae, C.S., Ambrose, J.A., Identification of vulnerable atherosclerotic plaques. Exp. Rev. Cardiovasc. Ther. 1:3 (2003), 353–365.
52. [52] Mancini, G.B.J., Dahlof, B., Diez, J., Surrogate markers for cardiovascular disease: structural markers. Circulation, 109(25 Suppl. 1), 2004, IV22-30.
53. [53] Ridker, P.M., Brown, N.J., Vaughan, D.E., Harrison, D.G., Mehta, J.L., Established and emerging plasma biomarkers in the prediction of first atherothrombotic events. Circulation, 109(25 Suppl. 1), 2004, IV6-19.
54. [54] Gibbons, G.H., Liew, C.C., Goodarzi, M.O., et al. Genetic markers: progress and potential for cardiovascular disease. Circulation, 109(25 Suppl. 1), 2004, IV47-58.
55. [55] Zhang, R., Xu, X., Chen, T., Li, L., Rao, P.F., An assay for angiotensin-converting enzyme using capillary zone electrophoresis. Anal. Biochem. 280:2 (2000), 286–290.
56. [56] Rigat, B., Hubert, C., Alhenc-Gelas, F., Cambien, F., Corvol, P., Soubrier, F., An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. J. Clin. Invest. 86:4 (1990), 1343–1346.
57. [57] Cambien, F., Poirier, O., Lecerf, L., et al. Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction. Nature 359:6396 (1992), 641–644.
58. [58] Keavney, B., McKenzie, C., Parish, S., et al. Large-scale test of hypothesised associations between the angiotensin-converting-enzyme insertion/deletion polymorphism and myocardial infarction in about 5000 cases and 6000 controls: International Studies of Infarct Survival (ISIS) collaborators. Lancet 355:9202 (2000), 434–442.
59. [59] Marian, A.J., Safavi, F., Ferlic, L., Dunn, J.K., Gotto, A.M., Ballantyne, C.M., Interactions between angiotensin-I converting enzyme insertion/deletion polymorphism and response of plasma lipids and coronary atherosclerosis to treatment with fluvastatin: the Lipoprotein and Coronary Atherosclerosis Study. J. Am. Coll. Cardiol. 35:1 (2000), 89–95.
60. [60] Schwartz, G.L., Turner, S.T., Chapman, A.B., et al. Interacting effects of gender and genotype on blood pressure response to hydrochlorothiazide. Kidney Int. 62:5 (2002), 1718–1723.
61. [61] Agema, W.R., Jukema, J.W., Zwinderman, A.H., van der Wall, E.E., A meta-analysis of the angiotensin-converting enzyme gene polymorphism and restenosis after percutaneous transluminal coronary revascularization: evidence for publication bias. Am. Heart J. 144:5 (2002), 760–768.
62. [62] Bonnici, F., Keavney, B., Collins, R., Danesh, J., Angiotensin converting enzyme insertion or deletion polymorphism and coronary restenosis: meta-analysis of 16 studies. BMJ 325:7363 (2002), 517–520.
63. [63] Jeunemaitre, X., Lifton, R.P., Hunt, S.C., Williams, R.R., Lalouel, J.M., Absence of linkage between the angiotensin converting enzyme locus and human essential hypertension. Nat. Genet. 1:1 (1992), 72–75.
64. [64] O'Donnell, C.J., Lindpaintner, K., Larson, M.G., et al. Evidence for association and genetic linkage of the angiotensin-converting enzyme locus with hypertension and blood pressure in men but not women in the Framingham Heart Study. Circulation 97:18 (1998), 1766–1772.
65. [65] Lindberg, M.K., Movérare, S., Skrtic, S., et al. Estrogen receptor (ER)-beta reduces ERalpha-regulated gene transcription, supporting a “ying yang” relationship between ERalpha and ERbeta in mice. Mol. Endocrinol. 17:2 (2003), 203–208.
66. [66] McInerney, E.M., Katzenellenbogen, B.S., Different regions in activation function-1 of the human estrogen receptor required for antiestrogen- and estradiol-dependent transcription activation. J. Biol. Chem. 271:39 (1996), 24172–24178.
67. [67] Elizabeth, M., Estrogen signaling and cardiovascular disease. Circ. Res. 109:6 (2011), 687–696.
68. [68] Anderson, G.L., Limacher, M., Assaf, A.R., et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA 291:14 (2004), 1701–1712.
69. [69] Rossouw, J.E., Anderson, G.L., Prentice, R.L., et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA 288:3 (2002), 321–333.
70. − mice. J. Clin. Invest. 107:3 (2001), 333–340.
71. [71] Wu, Q., Chambliss, K., Umetani, M., Mineo, C., Shaul, P.W., Non-nuclear estrogen receptor signaling in the endothelium. J. Biol. Chem. 286:17 (2011), 14737–14743.
72. [72] Meyer, M.R., Barton, M., ERalpha, ERbeta, and gpER: novel aspects of oestrogen receptor signalling in atherosclerosis. Cardiovasc. Res. 83:4 (2009), 605–610.
73. [73] Lenfant, F., Trémollieres, F., Gourdy, P., Arnal, J.F., Timing of the vascular actions of estrogens in experimental and human studies: why protective early, and not when delayed?. Maturitas 68:2 (2011), 165–173.
74. [74] Boerwinkle, E., Leffert, C.C., Lin, J., Lackner, C., Chiesa, G., Hobbs, H.H., Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J. Clin. Invest. 90:1 (1992), 52–60.
75. [75] Kamstrup, P.R., Tybjaerg-Hansen, A., Steffensen, R., Nordestgaard, B.G., Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 301:22 (2009), 2331–2339.
76. [76] Hobbs, H.H., White, A.L., Lipoprotein(a): intrigues and insights. Curr. Opin. Lipidol. 10:3 (1999), 225–236.
77. [77] Loscalzo, J., Weinfeld, M., Fless, G.M., et al. Lipoprotein(a), fibrin binding, and plasminogen activation. Arterioscler. Thromb. Vasc. Biol. 10:2 (1990), 240–245.
78. [78] Luc, G., Bard, J.M., Arveiler, D., et al. Lipoprotein(a) as a predictor of coronary heart disease: the PRIME study. Atherosclerosis 163:2 (2002), 377–384.
79. [79] von Eckardstein, A., Schulte, H., Cullen, P., Assmann, G., Lipoprotein(a) further increases the risk of coronary events in men with high global cardiovascular risk. J. Am. Coll. Cardiol. 37:2 (2001), 434–439.
80. [80] Kronenberg, F., Kronenberg, M.F., Kiechl, S., et al. Role of lipoprotein(a) and apolipoprotein(a) phenotype in atherogenesis: prospective results from the Bruneck study. Circulation 100:11 (1999), 1154–1160.
81. [81] Sharrett, A.R., Ballantyne, C.M., Coady, S.A., et al. Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein(a), apolipoproteins A-I and B, and HDL density subfractions: the Atherosclerosis Risk in Communities (ARIC) Study. Circulation 104:10 (2001), 1108–1113.
82. [82] Ariyo, A.A., Thach, C., Tracy, R., Lp(a) lipoprotein, vascular disease and mortality in the elderly. N. Engl. J. Med. 349:22 (2003), 2108–2115.
83. [83] Kuivenhoven, J.A., de Knijff, P., Boer, J.M., et al. Heterogeneity at the CETP gene locus: influence on plasma CETP concentrations and HDL cholesterol levels. Arterioscler. Thromb. Vasc. Biol. 17:3 (1997), 560–568.
84. [84] Kuivenhoven, J.A., Jukema, J.W., Zwinderman, A.H., et al. The role of a common variant of the cholesteryl ester transfer protein gene in the progression of coronary atherosclerosis: the Regression Growth Evaluation Statin Study Group. N. Engl. J. Med. 338:2 (1998), 86–93.
85. [85] Brousseau, M.E., O'Connor, J.J. Jr., Ordovas, J.M., et al. Cholesteryl ester transfer protein TaqI B2B2 genotype is associated with higher HDL cholesterol levels and lower risk of coronary heart disease end points in men with HDL deficiency: Veterans Affairs HDL Cholesterol Intervention Trial. Arterioscler. Thromb. Vasc. Biol. 22:7 (2002), 1148–1154.
86. [86] Ordovas, J.M., Cupples, L.A., Corella, D., et al. Association of cholesteryl ester transfer protein-TaqIB polymorphism with variations in lipoprotein subclasses and coronary heart disease risk: the Framingham study. Arterioscler. Thromb. Vasc. Biol. 20:5 (2000), 1323–1329.
87. [87] Sacks, F.M., Pfeffer, M.A., Moye, L.A., et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N. Engl. J. Med. 335:14 (1996), 1001–1009.
88. [88] de Grooth, G.J., Zerba, K.E., Huang, S.P., et al. The cholesteryl ester transfer protein (CETP) TaqIB polymorphism in the cholesterol and recurrent events study: no interaction with the response to pravastatin therapy and no effects on cardiovascular outcome: a prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy. J. Am. Coll. Cardiol. 43:5 (2004), 854–857.
89. [89] Agerholm-Larsen, B., Nordestgaard, B.G., Steffensen, R., Jensen, G., Tybjaerg-Hansen, A., Elevated HDL cholesterol is a risk factor for ischemic heart disease in white women when caused by a common mutation in the cholesteryl ester transfer protein gene. Circulation 101:16 (2000), 1907–1912.
90. [90] Agerholm-Larsen, B., Tybjaerg-Hansen, A., Schnohr, P., Steffensen, R., Nordestgaard, B.G., Common cholesteryl ester transfer protein mutations, decreased HDL cholesterol, and possible decreased risk of ischemic heart disease: the Copenhagen City heart study. Circulation 102:18 (2000), 2197–2203.
91. [91] Brattstrom, L., Wilcken, D.E., Ohrvik, J., Brudin, L., Common methylenetetrahydrolfolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis. Circulation 98:23 (1998), 2520–2526.
92. [92] Danesh, J., Lewington, S., Plasma homocysteine and coronary heart disease: systematic review of published epidemiological studies. J. Cardiovasc. Risk 5:4 (1998), 229–232.
93. [93] Klerk, M., Verhoef, P., Clarke, R., Blom, H.J., Kok, F.J., Schouten, E.G., MTHFR 677C → T polymorphism and risk of coronary heart disease: A meta-analysis. JAMA 288:11 (2002), 2023–2031.
94. [94] Kang, S.S., Zhou, J., Wong, P.W., Kowalisyn, J., Strokosch, G., Intermediate homocysteinemia: a thermolabile variant of methylenetetrahydrofolate reductase. Am. J. Hum. Genet. 43:4 (1988), 414–421.
95. [95] Frosst, P., Blom, H.J., Milos, R., et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nat. Genet. 10 (1995), 111–113.
96. [96] Poddar, R., Sivasubramanian, N., DiBello, P.M., Robinson, K., Jacobsen, D.W., Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells: implications for vascular disease. Circulation 103:22 (2001), 2717–2723.
97. [97] Jacques, P.F., Bostom, A.G., Wilson, P.W., Rich, S., Rosenberg, I.H., Selhub, J., Determinants of plasma total homocysteine concentration in the Framingham Offspring cohort. Am. J. Clin. Nutr. 73:3 (2001), 613–621.
98. [98] Michael, Y.T., Catherine, M.L., Jing, C., et al. Clinical utility of genotyping the 677C > T variant of methylenetetrahydrofolate reductase in humans is decreased in the post-folic acid fortification era. J. Nutr. 139:1 (2009), 33–37.
99. [99] Malinow, M.R., Nieto, F.J., Kruger, W.D., et al. The effects of folic acid supplementation on plasma total homocysteine are modulated by multivitamin use and methylenetetrahydrofolate reductase genotypes. Arterioscler. Thromb. Vasc. Biol. 17:6 (1997), 1157–1162.
100. [100] Saksela, O., Rifkin, D.B., Cell-associated plasminogen activation/regulation and physiological functions. Annu. Rev. Cell Biol. 4:1 (1998), 93–126.
101. [101] Fuster, V., Fayad, Z.A., Badimon, J.J., Acute coronary syndromes: biology. Lancet 353 (1999), SII5–SII9.
102. [102] Eren, M., Painter, C.A., Atkinson, J.B., Declerck, P.J., Vaughan, D.E., Age-dependent spontaneous coronary arterial thrombosis in transgenic mice that express a stable form of human plasminogen activator inhibitor-1. Circulation 106:4 (2002), 491–496.
103. [103] Dawson, S., Hamsten, A., Wiman, B., Henny, A., Humphries, S., Genetic variation at the plasminogen activator inhibitor-1 locus is associated with altered levels of plasma plasminogen activator-1 activity. Arterioscler. Thromb. Vasc. Biol. 11:1 (1991), 183–190.
104. [104] Festa, A., Agostino, R., Rich, S.S., Jenny, N.S., Tracy, R.P., Haffner, S.M., Promoter (4G/5G) plasminogen activator inhibitor-1 genotype and plasminogen activator inhibitor-1 levels in blacks, Hispanics, and non-Hispanic whites: the Insulin Resistance Atherosclerosis Study. Circulation 19 (2003), 2422–2427.
105. [105] Mansfield, M.W., Stickland, M.H., Grant, P.J., Environmental and genetic factors in relation to elevated circulating levels of plasminogen activator inhibitor-1 in Caucasian patients with non-insulin-dependent diabetes mellitus. Thromb. Haemost. 74:3 (1995), 842–847.
106. [106] Brown, N.J., Murphey, L.J., Srikuma, N., Koschachuhanan, N., Williams, G.H., Interactive effect of PAI-1 4G/5G genotype and salt intake on PAI-1 antigen. Arterioscler. Thromb. Vasc. Biol. 21:6 (2001), 1071–1077.
107. [107] Brown, N.J., Kumar, S., Painter, C.A., et al. ACE inhibition versus angiotensin type 1 receptor antagonism: differential effects on PAI-1 over time. Hypertension 40 (2002), 859–865.
108. [108] Hamsten, A., de Faire, U., Walldius, G., et al. Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet 330:8549 (1987), 3–9.
109. [109] Hamsten, A., Wiman, B., de Faire, U., Blomback, M., Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N. Engl. J. Med. 313:25 (1985), 1557–1563.
110. [110] Thogersen, A.M., Jansson, J.H., Boman, K., et al. High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women: evidence for the fibrinolytic system as an independent primary risk factor. Circulation 98:21 (1998), 2241–2247.
111. [111] Collet, J.P., Montalescot, G., Vicaut, E., et al. Acute release of plasminogen activator inhibitor-1 in ST-segment elevation myocardial infarction predicts mortality. Circulation 108:4 (2003), 391–394.
112. [112] Ridker, P.M., Vaughan, D.E., Stampfer, M.J., Endogenous tissue-type plasminogen activator and risk of myocardial infarction. Lancet 341:8854 (1993), 1165–1168.
113. [113] Michelson, A.D., Furman, M.I., Goldschmidt-Clermont, P., et al. Platelet GP IIIa Pl(A) polymorphisms display different sensitivities to agonists. Circulation 101:9 (2000), 1013–1018.
114. [114] Vickers, J.D., Binding of polymerizing fibrin to integrin alpha(IIb)beta(3) on chymotrypsin-treated rabbit platelets decreases phosphatidylinositol 4,5-bisphosphate and increases cytoskeletal actin”. Platelets 10:4 (1999), 228–237.
115. [115] Weiss, E.J., Bray, P.F., Tayback, M., et al. A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis. N. Engl. J. Med. 334:17 (1996), 1090–1094.
116. [116] Goldschmidt-Clermont, P.J., Shear, W.S., Schwartzberg, J., Varga, C.F., Bray, P.F., Clues to the death of an Olympic champion. Lancet, 347(9018), 1996, 1833.
117. [117] Carter, A.M., Ossei-Gerning, N., Grant, P.J., Platelet glycoprotein IIIa PlA polymorphism in young men with myocardial infarction. Lancet 348:9035 (1996), 485–486.
118. [118] Walter, D.H., Schachinger, V., Elsner, M., Dimmeler, S., Zeiher, A.M., Platelet glycoprotein IIIa polymorphisms and risk of coronary stent thrombosis. Lancet 350:9086 (1996), 1217–1219.
119. [119] Kastrati, A., Schomig, A., Seyfarth, M., et al. PlA polymorphism of platelet glycoprotein IIIa and risk of restenosis after coronary stent placement. Circulation 99:8 (1999), 1005–1010.
120. [120] Feng, D., Lindpaintner, K., Larson, M.G., et al. Increased platelet aggregability associated with platelet GPIIIa PlA2 polymorphism: the Framingham Offspring Study. Arterioscler. Thromb. Vasc. Biol. 19:4 (1999), 1142–1147.
121. [121] Ridker, P.M., Hennekens, C.H., Schmitz, C., Stampfer, M.J., Lindpaintner, K., PlA1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis. Lancet 349:4049 (1997), 385–388.
122. [122] Aleksic, N., Juneja, H., Folsom, A.R., et al. Platelet Pl(A2) allele and incidence of coronary heart disease: results from the Atherosclerosis Risk in Communities (ARIC) Study. Circulation 102:16 (2000), 1901–1905.
123. [123] Laule, M., Cascorbi, I., Stangl, V., et al. A1/A2 polymorphism of glycoprotein IIIa and association with excess procedural risk for coronary catheter interventions: a case–controlled study. Lancet 353:9154 (1999), 708–712.
124. [124] Lindmark, E., Diderholm, E., Wallentin, L., Siegbahn, A., Relationship between interleukin 6 and mortality in patients with unstable coronary artery disease: effects of an early invasive or noninvasive strategy. JAMA 286:17 (2001), 2107–2113.
125. [125] Albert, M.A., Danielson, E., Rifai, N., PRINCE investigators, effect of statin therapy on C-reactive protein levels: the Pravastatin Inflammation/CRP Evaluation (PRINCE): a randomized trial and cohort study. JAMA 286:1 (2001), 64–70.
126. [126] Ridker, P.M., Hennekens, C.H., Roitman-Johnson, B., Stampfer, M.J., Allen, J., Plasma concentration of soluble intercellular adhesion molecule 1 and risks of future myocardial infarction in apparently healthy men. Lancet 351:9096 (1998), 88–92.
127. [127] Ridker, P.M., Buring, J.E., Rifai, N., Soluble P-selectin and the risk of future cardiovascular events. Circulation 103:4 (2001), 491–495.
128. [128] Malik, I., Danesh, J., Whincup, P., et al. Soluble adhesion molecules and prediction of coronary heart disease: a prospective study and meta-analysis. Lancet 358:9286 (2001), 971–976.
129. [129] Schonbeck, U., Varo, N., Libby, P., Ridker, P.M., Soluble CD40L and cardiovascular risk in women. Circulation 104:19 (2001), 2266–2268.
130. [130] Heeschen, C., Dimmeler, S., Hamm, C.W., et al. Soluble CD40 ligand in acute coronary syndromes. N. Engl. J. Med. 348:12 (2003), 1104–1111.
131. [131] Packard, C.J., O'Reilly, D.S., Caslake, M.J., et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. West of Scotland Coronary Prevention Study Group. N. Engl. J. Med. 343:16 (2000), 1148–1155.
132. [132] Okamura, H., Tsutsi, H., Komatsu, T., et al. Cloning of a new cytokine that induces IFN-gamma production by T-cells. Nature 378:6552 (1995), 88–91.
133. [133] Galis, Z.S., Khatri, J.J., Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circ. Res. 90:3 (2002), 251–262.
134. [134] Hook, C.C., DiMagno, E.P., Tefferi, A., Primer on medical genomics, part XIII: ethical and regulatory issues. Mayo Clin. Proc. 79:5 (2004), 645–650.
135. [135] Hackett, J.L., Gutman, S.I., Introduction to the Food and Drug Administration (FDA) regulatory process. J. Proteome Res. 4:4 (2005), 1110–1113.
136. [136] Spence, J.D., Malinow, M.R., Barnett, P.A., Marian, A.J., Freeman, D., Hegele, R.A., Plasma homocyst(e)ine concentration, but not MTHFR genotype, is associated with variation in carotid plaque area. Stroke 30:5 (1999), 969–973.
137. [137] Ghilardi, G., Biondi, M.L., DeMonti, M., Turri, O., Guagnellini, E., Scorza, R., Matrix metalloproteinase-1 and matrix metalloproteinase-3 gene promoter polymorphisms are associated with carotid artery stenosis. Stroke 33:10 (2002), 2408–2412.
138. [138] Hou, L., Osei-Hyiaman, D., Yu, H., et al. Association of a 27-bp repeat polymorphism in ecNOS gene with ischemic stroke in Chinese patients. Neurology 56:4 (2001), 490–496.
139. [139] Morrison, A.C., Bray, M.S., Folsom, A.R., Boerwinkle, E., ADD1 460 W allele associated with cardiovascular disease in hypertensive individuals. Hypertension 39:6 (2002), 1053–1057.
140. [140] Nishiuma, S., Kario, K., Yakushijin, K., et al. Genetic variation in the promoter region of the beta-fibrinogen gene is associated with ischemic stroke in a Japanese population. Blood Coagul. Fibrinolysis 9:4 (1998), 373–379.
141. [141] Dai, K., Gao, W., Ruan, C., The Sma I polymorphism in the von Willebrand factor gene associated with acute ischemic stroke. Thromb. Res. 104:6 (2001), 389–395.
142. [142] Tang, D.C., Prauner, R., Liu, W., et al. Polymorphisms within the angiotensinogen gene (GT-repeat) and the risk of stroke in pediatric patients with sickle cell disease: a case–control study. Am. J. Hematol. 68:3 (2001), 164–169.
143. [143] Tan, K.T., Dempsey, A., Liew, C.C., Cardiac genes and gene databases for cardiovascular disease genetics. Curr. Hypertens. Rep. 1:1 (1999), 51–58.
144. [144] Kosachunhanun, N., Hunt, S.C., Hopkins, P.N., et al. Genetic determinants of nonmodulating hypertension. Hypertension 42:5 (2003), 901–908.
145. [145] Baker, E.H., Dong, Y.B., Sagnella, G.A., et al. Association of hypertension with T594M mutation in beta subunit of epithelial sodium channels in black people resident in London. Lancet 351:9113 (1998), 1388–1392.
146. [146] Cho, Y., Somer, B.G., Amatya, A., Natriuretic peptides and their therapeutic potential. Heart Dis. 1:5 (1999), 305–328.
147. [147] Rutherford, S., Johnson, M.P., Curtain, R.P., Griffiths, L.R., Chromosome 17 and the inducible nitric oxide synthase gene in human essential hypertension. Hum. Genet. 109:4 (2001), 408–415.
148. [148] Koschinsky, M.L., Boffa, M.B., Nesheim, M.E., et al. Association of a single nucleotide polymorphism in CPB2 encoding the thrombin-activatable fibrinolysis inhibitor (TAF1) with blood pressure. Clin. Genet. 60:5 (2001), 345–349.
149. [149] Davignon, J., Gregg, R.E., Sing, C.F., Apolipoprotein E polymorphism and atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 8:1 (1988), 1–21.
150. [150] Uzui, H., Harpf, A., Liu, M., et al. Increased expression of membrane type 3-matrix metalloproteinase in human atherosclerotic plaque: role of activated macrophages and inflammatory cytokines. Circulation 106:24 (2002), 3024–3030.
151. [151] Haddy, N., Sass, C., Droesch, S., et al. IL-6, TNF-alpha and atherosclerosis risk indicators in a healthy family population: the STANISLAS cohort. Atherosclerosis 170:2 (2003), 277–283.
152. [152] Stavljenic-Rukavina, A., Genetics of cardiovascular disease. J. Int. Fed. Clin. Chem, 2002 (Available at http://www.ifcc.org/ejifcc/vol14no2/ 140206200305n.htm).
153. [153] Gardeman, N.A., Stricker, J., Humme, J., et al. Angiotensinogen T174M and M235T gene polymorphisms are associated with the extent of coronary atherosclerosis. Atherosclerosis 145:2 (1999), 309–314.
154. [154] Rotter, J.I., Bu, X., Cantor, R.M., et al. Multilocus genetic determinants of LDL particle size in coronary artery disease families. Am. J. Hum. Genet. 58:3 (1996), 585–594.
155. [155] Ohtoshi, K., Yamasaki, Y., Gorogawa, S., et al. Association of (−)786T-C mutation of endothelial nitric oxide synthase gene with insulin resistance. Diabetologia 45:11 (2002), 1594–1601.
156. [156] Kubaszek, A., Pihlajamaki, J., Karhapaa, P., Vauhkonen, I., Laakso, M., The K121Q polymorphism of the PC-1 gene is associated with insulin resistance but not with dyslipidemia. Diabetes Care 26:2 (2003), 464–467.
157. [157] Ryan, A.S., Nicklas, B.J., Berman, D.M., Ferrel, R.E., The insertion/deletion polymorphism of the ACE gene is related to insulin sensitivity in overweight women. Diabetes Care 24:9 (2001), 1646–1652.
158. [158] Goodarzi, M.O., Guo, X., Taylor, K.D., et al. Lipoprotein lipase is a gene for insulin resistance in Mexican-Americans. Diabetes 53:1 (2004), 214–220.
159. [159] Bolla, M.K., Miller, G.J., Yellon, D.M., et al. Analysis of the association of a heat shock protein70–1 gene promoter polymorphism with myocardial infarction and coronary risk traits. Dis. Markers 13:4 (1998), 227–235.
160. [160] Sasaoka, T., Kimura, A., Hohta, S., Fakuda, N., Kurosawa, T., Izumi, T., Polymorphisms in the platelet endothelial cell adhesion molecule-1 (PECAM-1) gene, Asn563Ser and Gly670Arg, associated with myocardial infarction in the Japanese. Ann. N. Y. Acad. Sci. 947:1 (2001), 259–269.
161. [161] Terashima, M., Akita, H., Kanazawa, K., et al. Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction. Circulation 99:21 (1999), 2717–2719.
162. [162] Margaglione, M., Cappucci, G., Colaizzo, D., Vechione, G., Grandone, E., Di Moni, G., C-reactive protein in offspring is associated with the occurrence of myocardial infarction in first-degree relatives. Arterioscler. Thromb. Vasc. Biol. 20:1 (2000), 198–203.
163. [163] Batalla, A., Alvarez, R., Reguero, J.R., et al. Synergistic effect between apolipoprotein E and angiotensinogen gene polymorphisms in the risk for early myocardial infarction. Clin. Chem. 46:12 (2000), 1910–1915.
164. [164] Gonzalez, P., Alvarez, R., Batalla, A., et al. Genetic variation at the chemokine receptors CCR5/CCR2 in myocardial infarction. Genes Immunol. 2:4 (2001), 191–195.
165. [165] Holmer, S.R., Hengstenberg, C., Mayer, B., et al. Lipoprotein lipase gene polymorphism, cholesterol subfractions and myocardial infarction in large samples of the general population. Cardiovasc. Res. 47:4 (2000), 806–812.
166. [166] Cho, Y., Somer, B.G., Amatya, A., Natriuretic peptides and their therapeutic potential. Heart Dis. 1:5 (1999), 305–328.
167. [167] Hessner, M.J., Dinauer, D.M., Kwiatkowski, R., Neri, B., Raife, T.J., Age-dependent prevalence of vascular disease-associated polymorphisms among 2689 volunteer blood donors. Clin. Chem. 47:10 (2001), 1879–1884.
168. [168] Ferrarotti, I., Zorzetto, M., Beccaria, M., et al. Tumour necrosis factor family genes in a phenotype of COPD associated with emphysema. Eur. Respir. J. 21:3 (2003), 444–449.
169. [169] Francis, S.M., Larsen, J.E., Pavey, S.J., Bowman, R.V., Hayward, N.K., Fong, K.M., Yang, I.A., Expression profiling identifies genes involved in emphysema severity. Respir. Res. 10:1 (2009), 1–10.
170. [170] Higashi, K., Ishikawa, T., Ito, T., Yonemura, A., Shige, H., Nakamura, H., Association of a genetic variation in the beta 3-adrenergic receptor gene with coronary heart disease among Japanese. Biochem. Biophys. Res. Commun. 232:3 (1997), 728–730.
171. [171] Lacquemant, C., Lepretre, F., Pineda, I., et al. Mutation screening of the PPARalpha gene in type 2 diabetes associated with coronary heart disease. Diabetes Metab. 26:5 (2000), 393–401.
172. [172] Vickers, M.A., Green, F.R., Terry, C., et al. Genotype at a promoter polymorphism of the interleukin-6 gene is associated with baseline levels of plasma C-reactive protein. Cardiovasc. Res. 53:4 (2002), 1029–1034.
173. [173] Benes, P., Muzik, J., Benedik, J., et al. The C766T low-density lipoprotein receptor related protein polymorphism and coronary artery disease, plasma lipoproteins, and longevity in the Czech population. J. Mol. Med. 79:2–3 (2001), 116–120.
174. [174] Lin, R.C., Wang, X.L., Morris, B.J., Association of coronary artery disease with glucocorticoid receptor N363S variant. Hypertension 41:3 (2003), 404–407.
175. [175] Packard, C.J., O'Reilly, D.S., Caslake, M.J., et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. West of Scotland Coronary Prevention Study Group. N. Engl. J. Med. 343:6 (2000), 1148–1155.
176. [176] Rodriguez-Perez, J.C., Rodriguez-Esparragon, F., Hernandez-Perera, O., et al. Association of angiotensinogen M235T and A(-6)G gene polymorphisms with coronary heart disease with independence of essential hypertension: the PROCAGENE study. Prospective Cardiac Gene. J. Am. Coll. Cardiol. 37:6 (2001), 1536–1542.
177. [177] Stepanov, V.A., Puzyrev, V.P., Karpov, R.S., Kutmin, A., Genetic markers in coronary artery disease in a Russian population. Hum. Biol. 70:1 (1998), 47–57.
178. [178] von Beckerath, N., Schusterschitz, Y., Koch, W., et al. G protein beta 3 subunit 825T allele carriage and risk of coronary artery disease. Atherosclerosis 167:1 (2003), 135–139.
179. [179] Lovati, E., Richard, A., Frey, B.M., Ferry, F.J., Ferrari, O., Genetic polymorphisms of the renin-angiotensin-aldosterone system in end-stage renal disease. Kidney Int. 60:1 (2001), 46–54.
180. [180] Rossi, G.P., Taddei, S., Virdis, A., et al. The T-786C and Glu298Asp polymorphisms of the endothelial nitric oxide gene affect the forearm blood flow responses of Caucasian hypertensive patients. J. Am. Coll. Cardiol. 41:6 (2003), 938–945.
181. [181] Zhu, H., Sagnella, G.A., Dong, Y., et al. Contrasting associations between aldosterone synthase gene polymorphisms and essential hypertension in blacks and in whites. J. Hypertens. 21:1 (2003), 87–95.
182. [182] Nikitin, A.G., Gorashko, N.M., Minushkina, L.O., et al. Association of the G7831 A polymorphism of the ACE gene with myocardial ischemia in the Moscow population. Mol. Biol. (Mosk) 37:1 (2003), 54–56.
183. [183] Strauss, E., Waliszewski, K., Gabriel, M., Zapalski, S., Pawlak, A.L., Increased risk of the abdominal aortic aneurysm in carriers of the MTHFR 677T allele. J. Appl. Genet. 44:1 (2003), 85–93.
184. [184] Schillinger, M., Exner, M., Mlekusch, W., et al. Heme oxygenase-1 gene promoter polymorphism is associated with abdominal aortic aneurysm. Thromb. Res. 106:2 (2002), 131–136.
185. [185] Fortunato, G., Rubba, P., Panico, S., et al. A paraoxonase gene polymorphism, PON 1 (55), as an independent risk factor for increased carotid intima-media thickness in middle-aged women. Atherosclerosis 167:1 (2003), 141–148.
186. [186] Towbin, J.A., Bowles, N.E., The failing heart. Nature 415:6868 (2002), 227–233.