| [1] Pearson TA, Manolio TA. How to interpret a genome-wide association study. JAMA, 2008, 299(11): 1335–1344.
[2] Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet, 2006, 367(9524): 1747–1757.
[3] Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med, 2006, 3(11): e442.
[4] 卫生部心血管病防治研究中心.《中国心血管病防治报告2007》. 北京: 中国大百科全书出版社, 2009, 55–58.
[5] 卫生部心血管病防治研究中心.《中国心血管病防治报告2005》. 北京: 中国大百科全书出版社, 2006, 45–46.
[6] Ozaki K, Ohnishi Y, Iida A, Sekine A, Yamada R, Tsunoda T, Sato Hir, Sato Hid, Hori M, Nakamura Y, Tanaka T. Functional SNPs in the lymphotoxin-α gene that are asso-ciated with susceptibility to myocardial infarction. Nat Genet, 2002, 32(4): 650–654.
[7] The Wellcome Trust Case Control Consortium. Genome- wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature, 2007, 447(7145): 661–678.
[8] McPherson R, Pertsemlidis A, Kavaslar N, Stewart A, Roberts R, Cox DR, Hinds DA, Pennacchio LA, Tybjaerg- Hansen A, Folsom AR, Boerwinkle E, Hobbs HH, Cohen JC. A common allele on chromosome 9 associated with coronary heart disease. Science, 2007, 316(5830): 1488–1491.
[9] Helgadottir A, Thorleifsson G, Manolescu A, Gretarsdottir S, Blondal T, Jonasdottir A, Jonasdottir A, Sigurdsson A, Baker A, Palsson A, Masson G, Gudbjartsson DF, Magnusson KP, Andersen K, Levey AI, Backman VM, Matthiasdottir S, Jonsdottir T, Palsson S, Einarsdottir H, Gunnarsdottir S, Gylfason A, Vaccarino V, Hooper WC, Reilly MP, Granger CB, Austin H, Rader DJ, Shah SH, Quyyumi AA, Gulcher JR, Thorgeirsson G, Thorsteinsdottir U, Kong A, Stefansson K. A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science, 2007, 316(5830): 1491–1493.
[10] Larson MG, Atwood LD, Benjamin EJ, Cupples LA, D’Agostino RB Sr, Fox CS, Govindaraju DR, Guo CY, Heard-Costa NL, Hwang SJ, Murabito JM, Newton-Cheh C, O'Donnell CJ, Seshadri S, Vasan RS, Wang TJ, Wolf PA, Levy D. Framingham Heart Study 100K project: ge-nome-wide associations for cardiovascular disease out-comes. BMC Med Genet, 2007, 8 (Suppl. 1): S5.
[11] O'Donnell CJ, Cupples LA, D'Agostino RB, Fox CS, Hoffmann U, Hwang SJ, Ingellson E, Liu C, Murabito JM, Polak JF, Wolf PA, Demissie S. Genome-wide association study for subclinical atherosclerosis in major arterial ter-ritories in the NHLBI’s Framingham Hear Study. BMC Med Genet, 2007, 8 (Suppl. 1): S4.
[12] Samani NJ, Erdmann J, Hall AS, Hengstenberg C, Mangino M, Mayer B, Dixon RJ, Meitinger T, Braund P, Wichmann HE, Barrett JH, König IR, Stevens SE, Szymczak S, Tregouet DA, Iles MM, Pahlke F, Pollard H, Lieb W, Cambien F, Fischer M, Ouwehand W, Blankenberg S, Balmforth AJ, Baessler A, Ball SG, Strom TM, Braenne I, Gieger C, Deloukas P, Tobin MD, Ziegler A, Thompson JR, Schunkert H; WTCCC and the Cardiogenics Consortium. Genomewide association analysis of coronary artery disease. New Engl J Med, 2007, 357(5): 443–453.
[13] Fischer M, Broeckel U, Holmer S, Baessler A, Hengstenberg C, Mayer B, Erdmann J, Klein G, Riegger G, Jacob HJ, Schunkert H. Distinct heritable patterns of an-giographic coronary artery disease in families with myo-cardial infarction. Circulation, 2005, 111(7): 855–862.
[14] Dorn GW, Sharon Cresci. Genome-wide association stud-ies of coronary artery disease and heart failure: where are we going? Pharmacogenomics, 2009, 10(2): 213–223.
[15] Aulchenko YS, Ripatti S, Lindqvist I, Boomsma D, Heid IM, Pramstaller PP, Penninx BW, Janssens AC, Wilson JF, Spector T, Martin NG, Pedersen NL, Kyvik KO, Kaprio J, Hofman A, Freimer NB, |
