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Heart disease and stroke statistics - 2008 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee
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Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics - 2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008; 117: e25-e146.
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Circulation
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Rosamond, W.1
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A genome-wide association study for blood lipid phenotypes in the Framingham Heart study
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Kathiresan S, Manning A, Demissie S, et al. A genome-wide association study for blood lipid phenotypes in the Framingham Heart study. BMC Med Genet 2007; 8 (Suppl 1) : S17.
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Kathiresan, S.1
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Secreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic mice
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Lagace TA, Curtis DE, Garuti R, et al. Secreted PCSK9 decreases the number of LDL receptors in hepatocytes and in livers of parabiotic mice. J Clin Invest 2006;116:2995-3005.
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Lagace, T.A.1
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Mutations in PCSK9 cause autosomal dominant hypercholesterolemia
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Abifadel M, Varret M, Rabes J, et al. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nat Genet 2003;34:154-156.
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Abifadel, M.1
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Sequence variations in PCSK9, low LDL, and protection against coronary heart disease
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Cohen JC, Boerwinkle E, Mosley TH, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med 2006;354:1264-1272.
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Cohen, J.C.1
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6
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64249100539
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1st ed. Amsterdam and Boston: Elsevier/Academic Press
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Willard H. Genomic and personalized medicine. 1st ed. Amsterdam and Boston: Elsevier/Academic Press; 2009.
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Genomic and Personalized Medicine
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Willard, H.1
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7
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34249888775
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Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels
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Diabetes Genetics Initiative of Broad Institute of Harvard and MIT LU
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Diabetes Genetics Initiative of Broad Institute of Harvard and MIT LU; Saxena R, Voight BF, Lyssenko V, et al. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 2007;316:1331-1336.
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Science
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Saxena, R.1
Voight, B.F.2
Lyssenko, V.3
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8
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58149163149
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Common variants at 30 loci contribute to polygenic dyslipidemia
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Using GWA data from 19 840 individuals and targeted replication in up to 20 623 individuals, compelling statistical evidence is provided for 30 loci associated with LDL-C, HDL-C, and/or triglycerides
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Kathiresan S, Willer CJ, Peloso GM, et al. Common variants at 30 loci contribute to polygenic dyslipidemia. Nat Genet 2009;41:56-65. Using GWA data from 19 840 individuals and targeted replication in up to 20 623 individuals, compelling statistical evidence is provided for 30 loci associated with LDL-C, HDL-C, and/or triglycerides.
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Nat. Genet.
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Kathiresan, S.1
Willer, C.J.2
Peloso, G.M.3
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9
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58149161560
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Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts
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Using GWA data from 22 562 individuals, compelling statistical evidence is provided for 22 loci associated with LDL-C, HDL-C, and/or triglycerides. Almost all of these loci overlap with the work of Kathiresan et al. 8"
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Aulchenko YS, Ripatti S, Lindqvist I, et al. Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts. Nat Genet 2009;41:47-55. Using GWA data from 22 562 individuals, compelling statistical evidence is provided for 22 loci associated with LDL-C, HDL-C, and/or triglycerides. Almost all of these loci overlap with the work of Kathiresan et al. [8"].
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Nat. Genet.
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Aulchenko, Y.S.1
Ripatti, S.2
Lindqvist, I.3
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10
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33344464808
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A spectrum of PCSK9 alleles contributes to plasma levels of low-density lipoprotein cholesterol
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Kotowski IK, Pertsemlidis A, Luke A, et al. A spectrum of PCSK9 alleles contributes to plasma levels of low-density lipoprotein cholesterol. Am J Hum Genet 2006;78:410-422.
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Am. J. Hum Genet.
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Kotowski, I.K.1
Pertsemlidis, A.2
Luke, A.3
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11
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Polymorphisms associated with cholesterol and risk of cardiovascular events
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Kathiresan S, Melander O, Anevski D, et al. Polymorphisms associated with cholesterol and risk of cardiovascular events. N Engl J Med 2008;358:1240-1249.
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N. Engl. J. Med.
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Kathiresan, S.1
Melander, O.2
Anevski, D.3
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12
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36349016109
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Illuminating HDL: Is it still a viable therapeutic target?
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Rader DJ. Illuminating HDL: is it still a viable therapeutic target? N Engl J Med 2007;357:2180-2183.
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N. Engl. J. Med.
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Rader, D.J.1
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34247241088
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Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia
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Kastelein JJ, van Leuven SI, Burgess L, et al. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N Engl J Med 2007;356:1620-1630.
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N. Engl. J. Med.
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Kastelein, J.J.1
Van Leuven, S.I.2
Burgess, L.3
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34047106220
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Effect of torcetrapib on the progression of coronary atherosclerosis
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Nissen SE, Tardif J, Nicholls SJ, et al. Effect of torcetrapib on the progression of coronary atherosclerosis. N Engl J Med 2007;356:1304-1316.
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N. Engl. J. Med.
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Nissen, S.E.1
Tardif, J.2
Nicholls, S.J.3
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15
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58149262866
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A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection
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This study demonstrated that a nonsense mutation in apoC-III was associated with an improved lipoprotein profile and decreased coronary artery calcification
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Pollin TI, Damcott CM, Shen H, et al. A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection. Science 2008;322:1702-1705. This study demonstrated that a nonsense mutation in apoC-III was associated with an improved lipoprotein profile and decreased coronary artery calcification.
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Science
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Pollin, T.I.1
Damcott, C.M.2
Shen, H.3
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16
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58749087343
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Cardiovascular disease risk prediction with and without knowledge of genetic variation at chromosome 9p21.3
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This study showed that the use of genetic information for cardiovascular risk prediction did not offer any advantage over the use of serum lipids, CRP, and family history
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Paynter NP, Chasman DI, Buring JE, et al. Cardiovascular disease risk prediction with and without knowledge of genetic variation at chromosome 9p21.3. Ann Intern Med 2009;150:65-72. This study showed that the use of genetic information for cardiovascular risk prediction did not offer any advantage over the use of serum lipids, CRP, and family history.
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Ann. Intern. Med.
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Paynter, N.P.1
Chasman, D.I.2
Buring, J.E.3
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17
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69849094785
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Identification of genetic variants associated with response to statin therapy
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This genetic analysis from the PROVE-IT TIMI 22 trial demonstrated that specific isoforms of APOE were associated with a differential response to pravastatin or atorvastatin
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Mega JL, Morrow DA, Brown A, et al. Identification of genetic variants associated with response to statin therapy. Arterioscler Thromb Vasc Biol 2009;29:1310-1315. This genetic analysis from the PROVE-IT TIMI 22 trial demonstrated that specific isoforms of APOE were associated with a differential response to pravastatin or atorvastatin.
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Arterioscler Thromb. Vasc Biol.
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Mega, J.L.1
Morrow, D.A.2
Brown, A.3
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18
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69549111453
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Comprehensive whole-genome and candidate gene analysis for response to statin therapy in the Treating to New Targets (TNT) cohort
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*, certain APOE variants were significantly associated with statin response, as well as PCSK9 and HMGCR variants
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*], certain APOE variants were significantly associated with statin response, as well as PCSK9 and HMGCR variants.
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(2009)
Circ. Cardiovasc. Genet.
, vol.2
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Thompson, J.F.1
Hyde, C.L.2
Wood, L.S.3
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19
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49949104757
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SLCO1B1 variants and statin-induced myopathy: A genomewide study
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SEARCH Collaborative Group;, This study found that 60% of simvastatin-induced myopathy could be attributed to a variant in SLCO1B1, which encodes the organic anion transporter OATP1B1 that is responsible for the hepatic uptake of most statins
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The SEARCH Collaborative Group; Link E, Parish S, Armitage J, et al. SLCO1B1 variants and statin-induced myopathy: a genomewide study. N Engl J Med 2008;359:789-799. This study found that 60% of simvastatin-induced myopathy could be attributed to a variant in SLCO1B1, which encodes the organic anion transporter OATP1B1 that is responsible for the hepatic uptake of most statins.
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N. Engl. J. Med.
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Link, E.1
Parish, S.2
Armitage, J.3
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20
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70349739250
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*5 genetic variant is associated with statin-induced side effects
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This study found that the effect of SLCO1B1 variants did not signify the same risk of adverse events for all statins
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*5 genetic variant is associated with statin-induced side effects. J Am Coll Cardiol 2009;54:1609-1616. This study found that the effect of SLCO1B1 variants did not signify the same risk of adverse events for all statins.
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(2009)
J. Am. Coll. Cardiol.
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Voora, D.1
Shah, S.H.2
Spasojevic, I.3
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