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Genetics of Lipid Traits and Relationship to Coronary Artery Disease

  • Cardiovascular Genomics (C O'Donnell, Section Editor)
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Abstract

Despite the critical importance of plasma lipoproteins in the development of atherosclerosis, varying degrees of evidence surround the causal associations of lipoproteins with coronary artery disease (CAD). These causal contributions can be assessed by employing genetic variants as unbiased proxies for lipid levels. A relatively large number of low-density lipoprotein cholesterol (LDL-C) variants strongly associate with CAD, confirming the causal impact of this lipoprotein on atherosclerosis. Although not as firmly established, genetic evidence supporting a causal role of triglycerides (TG) in CAD is growing. Conversely, high-density lipoprotein cholesterol (HDL-C) variants not associated with LDL-C or TG have not yet been shown to be convincingly associated with CAD, raising questions about the causality of HDL-C in atherosclerosis. Finally, genetic variants at the LPA locus associated with lipoprotein(a) [Lp(a)] are decisively linked to CAD, indicating a causal role for Lp(a). Translational investigation of CAD-associated lipid variants may identify novel regulatory pathways with therapeutic potential to alter CAD risk.

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References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. Rader DJ, Daughtery A. Translating molecular discoveries into new therapies for atherosclerosis. Nature. 2008;451:904–13.

    Article  PubMed  CAS  Google Scholar 

  2. Rader DJ, Alexander ET, Weibel GL, et al. The role of reverse cholesterol transport in animals and humans and relationship to atherosclerosis. J Lipid Res. 2009;50S:189–94.

    Google Scholar 

  3. Di Angelantonio E, Sarwar N, et al. Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302:1993–2000.

    Article  PubMed  Google Scholar 

  4. Gotto Jr AM, Moon JE. Recent clinical studies of the effects of lipid-modifying therapies. Am J Cardiol. 2012;110:15A–26.

    Article  PubMed  CAS  Google Scholar 

  5. Wierzbicki AS, Clarke RE, Viljoen A, Mikhailidis DP. Triglycerides: a case for treatment? Curr Opin Cardiol. 2012;27:398–404.

    Article  PubMed  Google Scholar 

  6. Rader DJ, Tall AR. The not-so-simple HDL story: is it time to revise the HDL cholesterol hypothesis? Nat Med. 2012;18:1344–6.

    Article  PubMed  CAS  Google Scholar 

  7. Ebrahim S, Davey SG. Mendelian randomization: can genetic epidemiology help redress the failures of observational epidemiology? Hum Genet. 2008;123:15–33.

    Article  PubMed  Google Scholar 

  8. •• Teslovich TM, Musunuru K, Smith AV, et al. Biological, clinical and population relevance of 95 loci for blood lipids. Nature. 2010;466:707–13. This is the largest GWAS for lipid traits to date with over 100,000 individuals, and it also assessed association of lipid variants with CAD.

    Article  PubMed  CAS  Google Scholar 

  9. • Asselbergs FW, Guo Y, van Iperen EP, et al. Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci. Am J Hum Genet. 2012;91:823–38. This recent GWAS for lipid traits identified several new loci significantly associated with LDL-C, TG, HDL-C, and/or total cholesterol levels.

    Article  PubMed  CAS  Google Scholar 

  10. •• Deloukas P, Kanoni S, et al. The CARDIoGRAMplusC4D Consortium. Large-scale association analysis identifies new risk loci for coronary artery disease. Nat Genet. 2012;45:25–33. The largest GWAS for CAD to date found that over one-quarter of genome-wide significant CAD variants were also genome-wide significantly associated with lipid traits.

    Article  PubMed  Google Scholar 

  11. Kathiresan S, Srivastava D. Genetics of human cardiovascular disease. Cell. 2012;148:1242–57.

    Article  PubMed  CAS  Google Scholar 

  12. Rader DJ, Cohen J, Hobbs HH. Monogenic hyperchoelsterolemia: new insights in pathogenesis and treatment. J Clin Invest. 2003;111:1795–803.

    PubMed  CAS  Google Scholar 

  13. Marchini J, Howie B. Genotype imputation for genome-wide association studies. Nat Rev Genet. 2010;11:499–511.

    Article  PubMed  CAS  Google Scholar 

  14. Lawlor DA, Harbord RM, Sterne JA, et al. Mendelian randomization: using genes as instruments for making causal inferences in epidemiology. Stat Med. 2008;27:1133–63.

    Article  PubMed  Google Scholar 

  15. Strong A, Rader DJ. Clinical implications of lipid genetics for cardiovascular disease. Curr Cardiovasc Risk Rep. 2010;4:461–8.

    Article  PubMed  Google Scholar 

  16. •• Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a Mendelian randomization study. Lancet. 2012;380:572–80. The largest Mendelian randomization study of HDL-C and MI found that HDL-C raising genetic variants were not associated with a decreased risk of MI.

    Article  PubMed  CAS  Google Scholar 

  17. Whitfield AJ, Barrett PH, van Bockxmeer FM, et al. Lipid disorders and mutations in the APOB gene. Clin Chem. 2004;50:1725–32.

    Article  PubMed  CAS  Google Scholar 

  18. Shen H, Damcott CM, Rampersaud E, et al. Familial defective apoplipoprotein B-100 and increased low-density lipoprotein cholesterol and coronary artery calcification in the old order Amish. Arch Intern Med. 2010;170:1850–5.

    Article  PubMed  CAS  Google Scholar 

  19. Sankatsing RR, Fouchier SW, de Haan S, et al. Hepatic and cardiovascular consequences of familial hypobetalipoproteinemia. Arterioscler Thromb Vasc Biol. 2005;25:1979–84.

    Article  PubMed  CAS  Google Scholar 

  20. Fitzgerald ML, Mujawar Z, Tamehiro N. ABC transporters, atherosclerosis and inflammation. Atherosclerosis. 2010;211:361–70.

    Article  PubMed  CAS  Google Scholar 

  21. Hubacek JA, Berge KE, Cohen JC, Hobss HH. Mutations in ATP-cassette binding proteins G5 (ABCG5) and G8 (ABCG8) causing sitosterolemia. Human Mutat. 2001;18:359–60.

    Article  CAS  Google Scholar 

  22. Lee MH, Lu K, Patel SB. Genetic basis of sitosterolemia. Curr Opin Lipidol. 2001;12:141–9.

    Article  PubMed  CAS  Google Scholar 

  23. Abifadel M, Varret M, Rabes JP, et al. Mutations in PCSK9 cause autosomal dominant hypercholesterolemia. Nat Genet. 2003;34:154–6.

    Article  PubMed  CAS  Google Scholar 

  24. Humphries SE, Whittall RA, Hubbart CS, et al. Genetic causes of familial hypercholesterolaemia in patients in the UK: relation to plasma lipid levels and coronary heart disease risk. J Med Genet. 2006;43:943–9.

    Article  PubMed  CAS  Google Scholar 

  25. Cohen J, Pertsemlidis A, Kotowski IK, et al. Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9. Nat Genet. 2005;37:161–5.

    Article  PubMed  CAS  Google Scholar 

  26. Cohen JC, Boerwinkle E, Mosley Jr TH, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med. 2006;354:1264–72.

    Article  PubMed  CAS  Google Scholar 

  27. Zhang DW, Lagace TA, Garuti R, et al. Binding of proprotein convertase subtilisin/kexin type 9 to epidermal growth factor-like repeat A of low density lipoprotein receptor decreases receptor recycling and increases degradation. J Biol Chem. 2007;282:18602–12.

    Article  PubMed  CAS  Google Scholar 

  28. Fisher TS, Lo Surdo P, Pandit S, et al. Effects of pH and low density lipoprotein (LDL) on PCSK9-dependent LDL receptor regulation. J Biol Chem. 2007;282:20502–12.

    Article  PubMed  CAS  Google Scholar 

  29. Kathiresan S, Voight BF, et al. Myocardial Infarction Genetics Consortium. Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet. 2009;41:334–41.

    Article  PubMed  CAS  Google Scholar 

  30. Dias CS, Shaywitz AJ, Wasserman SM, et al. Effects of AMG 145 on low-density lipoprotein cholesterol levels: results from 2 randomized, double-blind, placebo-controlled, ascending-dose phase 1 studies in healthy volunteers and hypercholesterolemic subjects on statins. J Am Coll Cardiol. 2012;60:1888–98.

    Article  PubMed  CAS  Google Scholar 

  31. • Roth EM, McKenney JM, Hanotin C, et al. Atorvastatin with or without an antibody to PCSK9 in primary hypercholesterolemia. N Engl J Med. 2012;367:1891–900. This phase 2 randomized trial in patients with primary hypercholesterolemia showed that a PCSK9 monoclonal antibody added to a statin decreased LDL-C more than the statin alone.

    Article  PubMed  CAS  Google Scholar 

  32. Stein EA, Gipe D, Bergeron J, et al. Effect of a monoclonal antibody to PCSK9, REGN727/SAR236553, to reduce low-density lipoprotein cholesterol in patients with heterozygous familial hypercholesterolaemia on stable statin dose with or without ezetimibe therapy: a phase 2 randomized controlled trial. Lancet. 2012;380:29–36.

    Article  PubMed  CAS  Google Scholar 

  33. Kathiresan S, Melander O, Guiducci C, et al. Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans. Nat Genet. 2008;40:189–97.

    Article  PubMed  CAS  Google Scholar 

  34. Samani NJ, Erdmann J, Hall AS, et al. Genomewide association analysis of coronary artery disease. N Engl J Med. 2007;357:443–53.

    Article  PubMed  CAS  Google Scholar 

  35. •• Musunuru K, Strong A, Frank-Kamenetsky M, et al. From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus. Nature. 2010;466:714–9. This translational study demonstrated a functional mechanism by which a GWAS-identified lipid variant associated with CAD alters LDL-C levels.

    Article  PubMed  CAS  Google Scholar 

  36. Strong A, Ding Q, Edmondson AC, et al. Hepatic sortilin regulates both apolipoprotein B secretion and LDL catabolism. J Clin Invest. 2012;122:2807–16.

    Article  PubMed  CAS  Google Scholar 

  37. Reilly MP, Li M, He J, et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: 2 genome-wide association studies. Lancet. 2011;377:383–92.

    Article  PubMed  CAS  Google Scholar 

  38. Campos M, Sun W, Yu F, et al. Genetic determinants of plasma von Willebrand factor antigen levels: a target gene SNP and haplotype analysis of ARIC cohort. Blood. 2011;117:5224–30.

    Article  PubMed  CAS  Google Scholar 

  39. Zhang H, Mooney CJ, Reilly MP. ABO blood groups and cardiovascular diseases. Int J Vasc Med. 2012;2012:641917.

    PubMed  Google Scholar 

  40. Siest G, Pillot T, Regis-Bailly A, et al. Apolipoprotein E: an important gene and protein to follow in laboratory medicine. Clin Chem. 1995;41:1068–86.

    PubMed  CAS  Google Scholar 

  41. Mahley RW, Rall SC. Apolipoprotein E: far more than a lipid transport protein. Annu Rev Genomics Hum Genet. 2000;1:507–37.

    Article  PubMed  CAS  Google Scholar 

  42. Knouff C, Hinsdale ME, Mezdour H, et al. Apo E structure determines VLDL clearance and atherosclerosis risk in mice. J Clin Invest. 1999;103:1579–86.

    Article  PubMed  CAS  Google Scholar 

  43. van Dijk KW, Rensen PC, Voshol PJ, Havekes LM. The role and mode of action of apolipoproteins CIII and AV: synergistic actors in triglyceride metabolism? Curr Opin Lipidol. 2004;15:239–46.

    Article  PubMed  Google Scholar 

  44. O’Brien PJ, Alborn WE, Sloan JH, et al. The novel apolipoprotein A5 is present in human serum, is associated with VLDL, HDL, and chylomicrons, and circulates at very low concentrations compared with other apolipoproteins. Clin Chem. 2005;51:351–9.

    Article  PubMed  Google Scholar 

  45. Shachter NS. Apolipoproteins C-I and C-III as important modulators of lipoprotein metabolism. Curr Opin Lipidol. 2001;12:297–304.

    Article  PubMed  CAS  Google Scholar 

  46. Sundaram M, Zhong S, Bou Khalil M, et al. Expression of apolipoprotein C-III in McA-RH7777 cells enhances VLDL assembly and secretion under lipid-rich conditions. J Lipid Res. 2010;51:150–61.

    Article  PubMed  Google Scholar 

  47. Jong MC, Rensen PC, Dahlmans VE, et al. Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice. J Lipid Res. 2001;42:1578–85.

    PubMed  CAS  Google Scholar 

  48. Merkel M, Loeffler B, Kluger M, et al. Apolipoprotein AV accelerates plasma hydrolysis of triglyceride-rich lipoproteins by interaction with proteoglycan-bound lipoprotein lipase. J Biol Chem. 2005;280:21553–60.

    Article  PubMed  CAS  Google Scholar 

  49. Schaap FG, Rensen PC, Voshol PJ, et al. ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglyceride (VLDL-TG) production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis. J Biol Chem. 2004;279:27941–7.

    Article  PubMed  CAS  Google Scholar 

  50. Ito Y, Azrolan N, O’Connell A, et al. Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Science. 1990;249:790–3.

    Article  PubMed  CAS  Google Scholar 

  51. van der Vliet HN, Schaap FG, Levels JH, et al. Adenoviral overexpression of apolipoprotein A-V reduces serum levels of triglycerides and cholesterol in mice. Biochem Biophys Res Commun. 2002;295:1156–9.

    Article  PubMed  Google Scholar 

  52. Varbo A, Benn M, Tybjaerg-Hansen A, et al. TRIB1 and GCKR polymorphisms, lipid levels, and risk of ischemic heart disease in the general population. Arterioscler Thromb Vasc Biol. 2011;31:451–7.

    Article  PubMed  CAS  Google Scholar 

  53. • Burkhardt R, Toh SA, Lagor WR, et al. Trib1 is a lipid- and myocardial infarction-associated gene that regulates hepatic lipogenesis and VLDL production in mice. J Clin Invest. 2010;120:4410–4. Motivated by GWAS results, this study found that overexpression of hepatic TRIB1 decreased plasma TG in mice and that TRIB1 knockout mice demonstrated increased plasma TG, suggesting that the TRIB1 gene is a novel regulator of TG metabolism.

    Article  PubMed  CAS  Google Scholar 

  54. Mattijssen F, Kersten S. Regulation of triglyceride metabolism by angiopoietin-like proteins. Biochim Biophys Acta. 1821;2012:782–9.

    Google Scholar 

  55. • Musunuru K, Pirruccello JP, Do R, et al. Exome sequencing, ANGPTL3 mutations, and familial combined hypolipidemia. N Engl J Med. 2010;363:2220–7. This exome sequencing study identified 2 nonsense mutations in ANGPTL3 that influence lipid metabolism.

    Article  PubMed  CAS  Google Scholar 

  56. Shimizugawa T, Ono M, Shimamura M, et al. ANGPTL3 decreases very low density lipoprotein triglyceride clearance by inhibition of lipoprotein lipase. J Biol Chem. 2002;277:33742–8.

    Article  PubMed  CAS  Google Scholar 

  57. Shan L, Yu XC, Liu Z, et al. The angiopoietin-like proteins ANGPTL3 and ANGPTL4 inhibit lipoprotein lipase activity through distinct mechanisms. J Biol Chem. 2009;284:1419–24.

    Article  PubMed  CAS  Google Scholar 

  58. Koster A, Chao YB, Mosior M, et al. Transgenic angiopoietin-like (angptl)4 overexpression and targeted disruption of angptl4 and angptl3: regulation of triglyceride metabolism. Endocrinology. 2005;146:4943–50.

    Article  PubMed  CAS  Google Scholar 

  59. Kirchgessner TG, LeBoeuf RC, Langner CA, et al. Genetic and developmental regulation of the lipoprotein lipase gene: loci both distal and proximal to the lipoprotein lipase structural gene control enzyme expression. J Biol Chem. 1989;264:1473–82.

    PubMed  CAS  Google Scholar 

  60. Havel RJ. Triglyceride-rich lipoproteins and plasma lipid transport. Arterioscler Thromb Vasc Biol. 2010;30:9–19.

    Article  PubMed  CAS  Google Scholar 

  61. Myers Jr MG, Sun XJ, White MF. The IRS-1 signaling system. Trends Biochem Sci. 1994;19:289–93.

    Article  PubMed  CAS  Google Scholar 

  62. Rung J, Cauchi S, Albrechtsen A, et al. Genetic variant near IRS1 is associated with type 2 diabetes, insulin resistance and hyperinsulinemia. Nat Genet. 2009;41:1110–5.

    Article  PubMed  CAS  Google Scholar 

  63. Sim E, Fakis G, Laurieri N, Boukouvala S. Arylamine N-acetyltransferases–from drug metabolism and pharmacogenetics to identification of novel targets for pharmacological intervention. Adv Pharmacol. 2012;63:169–205.

    Article  PubMed  CAS  Google Scholar 

  64. Rader DJ, de Goma EM. Approach to the patient with extremely low HDL-cholesterol. J Clin Endocrinol Metab. 2012;97:3399–407.

    Article  PubMed  CAS  Google Scholar 

  65. Rader DJ. Regulation of reverse cholesterol transport and clinical implications. Am J Cardiol. 2003;92:42J–9.

    Article  PubMed  CAS  Google Scholar 

  66. de Lemos AS, Wolfe ML, Long CJ, et al. Identification of genetic variants in endothelial lipase in persons with elevated high-density lipoprotein cholesterol. Circulation. 2002;106:1321–6.

    Article  Google Scholar 

  67. Edmondson AC, Brown RJ, Kathiresan S, et al. Loss-of-function variants in endothelial lipase are a cause of elevated HDL cholesterol in humans. J Clin Invest. 2009;119:1042–50.

    PubMed  CAS  Google Scholar 

  68. • Haase CL, Tybjaerg-Hansen A, Qayyum AA, Schou J, Nordestgaard BG, Frikke-Schmidt R. LCAT, HDL cholesterol, and ischemic cardiovascular disease: a Mendelian randomization study of HDL cholesterol in 54,500 individuals. J Clin Endocrinol Metab. 2012;97:248–56. This Mendelian randomization study showed that a lecithin-cholesterol acyltransferase variant was significantly associated with decreased HDL-C levels but not with increased risk of MI.

    Article  Google Scholar 

  69. Johannsen TH, Kamstrup PR, Andersen RV, et al. Hepatic lipase, genetically elevated high-density lipoprotein, and risk of ischemic cardiovascular disease. J Clin Endocrinol Metab. 2009;94:1264–73.

    Article  PubMed  CAS  Google Scholar 

  70. Andersen RV, Wittrup HH, Tybjaerg-Hansen A, et al. Hepatic lipase mutations, elevated high-density lipoprotein cholesterol, and increased risk of ischemic heart disease: the Copenhagen city heart study. J Am Coll Cardiol. 2003;41:1972–82.

    Article  PubMed  CAS  Google Scholar 

  71. Frikke-Schmidt R, Nordestgaard BG, Stene MC, et al. Association of loss-of-function mutations in the ABCA1 gene with high-density lipoprotein cholesterol levels and risk of ischemic heart disease. JAMA. 2008;299:2524–32.

    Article  PubMed  CAS  Google Scholar 

  72. Frikke-Schmidt R, Nordestgaard BG, Jensen GB, et al. Genetic variation in ABCA1 predicts ischemic heart disease in the general population. Arterioscler Thromb Vasc Biol. 2008;28:180–6.

    Article  PubMed  CAS  Google Scholar 

  73. Thompson A, Di Angelantonio E, Sarwar N, et al. Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk. JAMA. 2008;299:2777–88.

    Article  PubMed  CAS  Google Scholar 

  74. Boekholdt SM, Sacks FM, Jukema JW, et al. Cholesteryl ester transfer protein TaqIB variant, high-density lipoprotein cholesterol levels, cardiovascular risk, and efficacy of pravastatin treatment: individual patient meta-analysis of 13,677 subjects. Circulation. 2005;111:278–87.

    Article  PubMed  CAS  Google Scholar 

  75. Larach DB, de Goma EM, Rader DJ. Targeting high density lipoproteins in the prevention of cardiovascular disease? Curr Cardiol Rep. 2012;14:684–91.

    Article  PubMed  Google Scholar 

  76. • Tsimikas S, Hall JL. Lipoprotein(a) as a potential causal genetic risk factor of cardiovascular disease: a rationale for increased efforts to understand its pathophysiology and develop targeted therapies. J Am Coll Cardiol. 2012;60:716–21. This review summarizes in detail the leading hypothesized mechanisms linking Lp(a) to cardiovascular disease.

    Article  PubMed  CAS  Google Scholar 

  77. Lamon-Fava S, Jimenez D, Christian JC, et al. The NHLBI Twin Study: heritability of apolipoprotein A-I and B, and low density lipoprotein subclasses and concordance for lipoprotein(a). Atherosclerosis. 1991;91:97–106.

    Article  PubMed  CAS  Google Scholar 

  78. Kronenberg F, Utermann G. Lipoprotein(a): resurrected by genetics. J Intern Med. 2012;273:6–30.

    Article  PubMed  Google Scholar 

  79. Li KM, Wilcken DE, Dudman NP. Effect of serum lipoprotein (a) on estimation of low-density lipoprotein cholesterol by the Friedewald formula. Clin Chem. 1994;40:571–3.

    PubMed  CAS  Google Scholar 

  80. Clarke R, Peden JF, Hopewell JC, et al. Genetic variants associated with lp(a) lipoprotein level and coronary disease. N Engl J Med. 2009;361:2518–28.

    Article  PubMed  CAS  Google Scholar 

  81. Dube JB, Boffa MB, Hegele RA, Koschinsky ML. Lipoprotein(a): more interesting than ever after 50 years. Curr Opin Lipidol. 2012;23:133–40.

    Article  PubMed  CAS  Google Scholar 

  82. • Li Y, Luke MM, Shiffman D, Devlin JJ. Genetic variants in the apolipoprotein(a) gene and coronary heart disease. Circ Cardiovasc Genet. 2011;4:565–73. This meta-analysis found that 2 SNPs in the LPA gene are independently associated with Lp(a) levels and CAD..

    Article  PubMed  CAS  Google Scholar 

  83. Helgadottir A, Gretarsdottir S, Thorleifsson G, et al. Apolipoprotein(a) genetic sequence variants associated with systemic atherosclerosis and coronary atherosclerotic burden but not with venous thromboembolism. J Am Coll Cardiol. 2012;60:722–9.

    Article  PubMed  CAS  Google Scholar 

  84. Bergmark C, Dewan A, Orsoni A, et al. A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma. J Lipid Res. 2008;49:2230–9.

    Article  PubMed  CAS  Google Scholar 

  85. Seimon TA, Nadolski MJ, Liao X, et al. Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress. Cell Metab. 2010;12:467–82.

    Article  PubMed  CAS  Google Scholar 

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Tanya E. Keenan declares that she has no conflict of interest. Daniel J. Rader declares that he has no conflict of interest.

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  1. Perelman School of Medicine at the University of Pennsylvania, 8044 Maloney Building, 3400 Spruce St, Philadelphia, PA, 19104, USA

    Tanya E. Keenan

  2. Cardiovascular Institute and Institute for Translational Medicine and Therapeutics, Perelman School of Medicine at the University of Pennsylvania, 11-125 TRC, 3400 Civic Center Blvd, Philadelphia, PA, 19104, USA

    Daniel J. Rader

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  1. Tanya E. Keenan
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Correspondence to Daniel J. Rader.

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Keenan, T.E., Rader, D.J. Genetics of Lipid Traits and Relationship to Coronary Artery Disease. Curr Cardiol Rep 15, 396 (2013). https://doi.org/10.1007/s11886-013-0396-9

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