Connor A Emdin1, Amit V Khera1, Pradeep Natarajan1, Derek Klarin1, Hong-Hee Won2, Gina M Peloso3, Nathan O Stitziel4, Akihiro Nomura1, Seyedeh M Zekavat1, Alexander G Bick5, Namrata Gupta5, Rosanna Asselta6, Stefano Duga6, Piera Angelica Merlini7, Adolfo Correa8, Thorsten Kessler9, James G Wilson10, Matthew J Bown11, Alistair S Hall12, Peter S Braund11, Nilesh J Samani11, Heribert Schunkert13, Jaume Marrugat14, Roberto Elosua14, Ruth McPherson15, Martin Farrall16, Hugh Watkins16, Cristen Willer17, Gonçalo R Abecasis18, Janine F Felix19, Ramachandran S Vasan20, Eric Lander5, Daniel J Rader21, John Danesh22, Diego Ardissino23, Stacey Gabriel5, Danish Saleheen24, Sekar Kathiresan25. 1. Center for Human Genetic Research, Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. 2. Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Medical Center, Seoul, Republic of Korea. 3. Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. 4. Departments of Medicine, Genetics, and the McDonnell Genome Institute, Washington University School of Medicine, St. Louis, Missouri. 5. Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. 6. Department of Biomedical Sciences, Humanitas University and Humanitas Clinical and Research Center, Milan, Italy. 7. Ospedale Niguarda, Milan, Italy. 8. Jackson Heart Study, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi. 9. Deutsches Herzzentrum München, Technische Universität München, Deutsches Zentrum für Herz-Kreislauf-Forschung, München, Germany; Munich Heart Alliance, München, Germany. 10. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi. 11. Departments of Cardiovascular Sciences and NIHR Leicester Cardiovascular Biomedical Research Unit, University of Leicester, Leicester, United Kingdom. 12. Leeds Institute of Cardiovascular and Metabolic Medicine, Leeds University, Leeds, United Kingdom. 13. Deutsches Herzzentrum München, Technische Universität München, Deutsches Zentrum für Herz-Kreislauf-Forschung, München, Germany. 14. Cardiovascular Epidemiology & Genetics, IMIM (Hospital del Mar Research Institute), Barcelona, Spain. 15. University of Ottawa Heart Institute, Ottawa, Ontario, Canada. 16. Division of Cardiovascular Medicine, Radcliffe Department of Medicine and the Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom. 17. Department of Computational Medicine and Bioinformatics, Department of Human Genetics, and Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan. 18. Center for Statistical Genetics, Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, Michigan. 19. Department of Epidemiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands. 20. National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Sections of Cardiology, Preventive Medicine and Epidemiology, Department of Medicine, Boston University Schools of Medicine and Public Health, Boston, Massachusetts. 21. Department of Genetics, University of Pennsylvania, Philadelphia, Pennsylvania. 22. Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom; National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. 23. Division of Cardiology, Azienda Ospedaliero-Universitaria di Parma, University of Parma, Parma, Italy; ASTC: Associazione per lo Studio Della Trombosi in Cardiologia, Pavia, Italy. 24. Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 25. Center for Human Genetic Research, Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. Electronic address: skathiresan1@mgh.harvard.edu.
Abstract
BACKGROUND: Genomic analyses have suggested that the LPA gene and its associated plasma biomarker, lipoprotein(a) (Lp[a]), represent a causal risk factor for coronary heart disease (CHD). As such, lowering Lp(a) levels has emerged as a therapeutic strategy. Beyond target identification, human genetics may contribute to the development of new therapies by defining the full spectrum of beneficial and adverse consequences and by developing a dose-response curve of target perturbation. OBJECTIVES: The goal of this study was to establish the full phenotypic impact of LPA gene variation and to estimate a dose-response curve between genetically altered plasma Lp(a) and risk for CHD. METHODS: We leveraged genetic variants at the LPA gene from 3 data sources: individual-level data from 112,338 participants in the U.K. Biobank; summary association results from large-scale genome-wide association studies; and LPA gene sequencing results from case subjects with CHD and control subjects free of CHD. RESULTS: One SD genetically lowered Lp(a) level was associated with a 29% lower risk of CHD (odds ratio [OR]: 0.71; 95% confidence interval [CI]: 0.69 to 0.73), a 31% lower risk of peripheral vascular disease (OR: 0.69; 95% CI: 0.59 to 0.80), a 13% lower risk of stroke (OR: 0.87; 95% CI: 0.79 to 0.96), a 17% lower risk of heart failure (OR: 0.83; 95% CI: 0.73 to 0.94), and a 37% lower risk of aortic stenosis (OR: 0.63; 95% CI: 0.47 to 0.83). We observed no association with 31 other disorders, including type 2 diabetes and cancer. Variants that led to gain of LPA gene function increased the risk for CHD, whereas those that led to loss of gene function reduced the CHD risk. CONCLUSIONS: Beyond CHD, genetically lowered Lp(a) levels are associated with a lower risk of peripheral vascular disease, stroke, heart failure, and aortic stenosis. As such, pharmacological lowering of plasma Lp(a) may influence a range of atherosclerosis-related diseases.
BACKGROUND: Genomic analyses have suggested that the LPA gene and its associated plasma biomarker, lipoprotein(a) (Lp[a]), represent a causal risk factor for coronary heart disease (CHD). As such, lowering Lp(a) levels has emerged as a therapeutic strategy. Beyond target identification, human genetics may contribute to the development of new therapies by defining the full spectrum of beneficial and adverse consequences and by developing a dose-response curve of target perturbation. OBJECTIVES: The goal of this study was to establish the full phenotypic impact of LPA gene variation and to estimate a dose-response curve between genetically altered plasma Lp(a) and risk for CHD. METHODS: We leveraged genetic variants at the LPA gene from 3 data sources: individual-level data from 112,338 participants in the U.K. Biobank; summary association results from large-scale genome-wide association studies; and LPA gene sequencing results from case subjects with CHD and control subjects free of CHD. RESULTS: One SD genetically lowered Lp(a) level was associated with a 29% lower risk of CHD (odds ratio [OR]: 0.71; 95% confidence interval [CI]: 0.69 to 0.73), a 31% lower risk of peripheral vascular disease (OR: 0.69; 95% CI: 0.59 to 0.80), a 13% lower risk of stroke (OR: 0.87; 95% CI: 0.79 to 0.96), a 17% lower risk of heart failure (OR: 0.83; 95% CI: 0.73 to 0.94), and a 37% lower risk of aortic stenosis (OR: 0.63; 95% CI: 0.47 to 0.83). We observed no association with 31 other disorders, including type 2 diabetes and cancer. Variants that led to gain of LPA gene function increased the risk for CHD, whereas those that led to loss of gene function reduced the CHD risk. CONCLUSIONS: Beyond CHD, genetically lowered Lp(a) levels are associated with a lower risk of peripheral vascular disease, stroke, heart failure, and aortic stenosis. As such, pharmacological lowering of plasma Lp(a) may influence a range of atherosclerosis-related diseases.
Authors: Nicholas L Smith; Janine F Felix; Alanna C Morrison; Serkalem Demissie; Nicole L Glazer; Laura R Loehr; L Adrienne Cupples; Abbas Dehghan; Thomas Lumley; Wayne D Rosamond; Wolfgang Lieb; Fernando Rivadeneira; Joshua C Bis; Aaron R Folsom; Emelia Benjamin; Yurii S Aulchenko; Talin Haritunians; David Couper; Joanne Murabito; Ying A Wang; Bruno H Stricker; John S Gottdiener; Patricia P Chang; Thomas J Wang; Kenneth M Rice; Albert Hofman; Susan R Heckbert; Ervin R Fox; Christopher J O'Donnell; Andre G Uitterlinden; Jerome I Rotter; James T Willerson; Daniel Levy; Cornelia M van Duijn; Bruce M Psaty; Jacqueline C M Witteman; Eric Boerwinkle; Ramachandran S Vasan Journal: Circ Cardiovasc Genet Date: 2010-05-05
Authors: A R Sharrett; C M Ballantyne; S A Coady; G Heiss; P D Sorlie; D Catellier; W Patsch Journal: Circulation Date: 2001-09-04 Impact factor: 29.690
Authors: Sotirios Tsimikas; Nicholas J Viney; Steven G Hughes; Walter Singleton; Mark J Graham; Brenda F Baker; Jennifer L Burkey; Qingqing Yang; Santica M Marcovina; Richard S Geary; Rosanne M Crooke; Joseph L Witztum Journal: Lancet Date: 2015-07-22 Impact factor: 79.321
Authors: C Sandholzer; N Saha; J D Kark; A Rees; W Jaross; H Dieplinger; F Hoppichler; E Boerwinkle; G Utermann Journal: Arterioscler Thromb Date: 1992-10
Authors: Amit V Khera; Hong-Hee Won; Gina M Peloso; Kim S Lawson; Traci M Bartz; Xuan Deng; Elisabeth M van Leeuwen; Pradeep Natarajan; Connor A Emdin; Alexander G Bick; Alanna C Morrison; Jennifer A Brody; Namrata Gupta; Akihiro Nomura; Thorsten Kessler; Stefano Duga; Joshua C Bis; Cornelia M van Duijn; L Adrienne Cupples; Bruce Psaty; Daniel J Rader; John Danesh; Heribert Schunkert; Ruth McPherson; Martin Farrall; Hugh Watkins; Eric Lander; James G Wilson; Adolfo Correa; Eric Boerwinkle; Piera Angelica Merlini; Diego Ardissino; Danish Saleheen; Stacey Gabriel; Sekar Kathiresan Journal: J Am Coll Cardiol Date: 2016-04-03 Impact factor: 24.094
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