J Gustav Smith1, Kevin Luk2, Christina-Alexandra Schulz3, James C Engert4, Ron Do5, George Hindy3, Gull Rukh3, Line Dufresne2, Peter Almgren3, David S Owens6, Tamara B Harris7, Gina M Peloso8, Kathleen F Kerr9, Quenna Wong9, Albert V Smith10, Matthew J Budoff11, Jerome I Rotter11, L Adrienne Cupples12, Stephen Rich13, Sekar Kathiresan14, Marju Orho-Melander3, Vilmundur Gudnason10, Christopher J O'Donnell15, Wendy S Post16, George Thanassoulis4. 1. Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden2Department of Heart Failure and Valvular Disease, Skåne University Hospital, Lund, Sweden3Department of Clinical Sciences, Lund University, Malmö, Sweden4Program in Medical and Pop. 2. McGill University Health Center, Preventive and Genomic Cardiology, Montreal, Quebec, Canada. 3. Department of Clinical Sciences, Lund University, Malmö, Sweden. 4. McGill University Health Center, Preventive and Genomic Cardiology, Montreal, Quebec, Canada6McGill University Health Center and Research Institute, Department of Medicine, Montreal, Quebec, Canada. 5. Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston. 6. Department of Medicine, University of Washington, Seattle. 7. National Institute on Aging, Bethesda, Maryland. 8. Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts. 9. Department of Biostatistics, University of Washington, Seattle. 10. Icelandic Heart Association Research Institute, Kopavogur, Iceland12Faculty of Medicine, University of Iceland, Reykjavik, Iceland. 11. Los Angeles Biomedical Research Institute at Harbor-UCLA, Los Angeles, California. 12. Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts15Framingham Heart Study, Framingham, Massachusetts. 13. University of Virginia, Charlottesville. 14. Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts7Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston17Cardiology Division, Massachusetts General Hospi. 15. Framingham Heart Study, Framingham, Massachusetts17Cardiology Division, Massachusetts General Hospital, Boston18NHLBI Cardiovascular Epidemiology and Human Genomics Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland. 16. Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
Abstract
IMPORTANCE: Plasma low-density lipoprotein cholesterol (LDL-C) has been associated with aortic stenosis in observational studies; however, randomized trials with cholesterol-lowering therapies in individuals with established valve disease have failed to demonstrate reduced disease progression. OBJECTIVE: To evaluate whether genetic data are consistent with an association between LDL-C, high-density lipoprotein cholesterol (HDL-C), or triglycerides (TG) and aortic valve disease. DESIGN, SETTING, AND PARTICIPANTS: Using a Mendelian randomization study design, we evaluated whether weighted genetic risk scores (GRSs), a measure of the genetic predisposition to elevations in plasma lipids, constructed using single-nucleotide polymorphisms identified in genome-wide association studies for plasma lipids, were associated with aortic valve disease. We included community-based cohorts participating in the CHARGE consortium (n = 6942), including the Framingham Heart Study (cohort inception to last follow-up: 1971-2013; n = 1295), Multi-Ethnic Study of Atherosclerosis (2000-2012; n = 2527), Age Gene/Environment Study-Reykjavik (2000-2012; n = 3120), and the Malmö Diet and Cancer Study (MDCS, 1991-2010; n = 28,461). MAIN OUTCOMES AND MEASURES: Aortic valve calcium quantified by computed tomography in CHARGE and incident aortic stenosis in the MDCS. RESULTS: The prevalence of aortic valve calcium across the 3 CHARGE cohorts was 32% (n = 2245). In the MDCS, over a median follow-up time of 16.1 years, aortic stenosis developed in 17 per 1000 participants (n = 473) and aortic valve replacement for aortic stenosis occurred in 7 per 1000 (n = 205). Plasma LDL-C, but not HDL-C or TG, was significantly associated with incident aortic stenosis (hazard ratio [HR] per mmol/L, 1.28; 95% CI, 1.04-1.57; P = .02; aortic stenosis incidence: 1.3% and 2.4% in lowest and highest LDL-C quartiles, respectively). The LDL-C GRS, but not HDL-C or TG GRS, was significantly associated with presence of aortic valve calcium in CHARGE (odds ratio [OR] per GRS increment, 1.38; 95% CI, 1.09-1.74; P = .007) and with incident aortic stenosis in MDCS (HR per GRS increment, 2.78; 95% CI, 1.22-6.37; P = .02; aortic stenosis incidence: 1.9% and 2.6% in lowest and highest GRS quartiles, respectively). In sensitivity analyses excluding variants weakly associated with HDL-C or TG, the LDL-C GRS remained associated with aortic valve calcium (P = .03) and aortic stenosis (P = .009). In instrumental variable analysis, LDL-C was associated with an increase in the risk of incident aortic stenosis (HR per mmol/L, 1.51; 95% CI, 1.07-2.14; P = .02). CONCLUSIONS AND RELEVANCE: Genetic predisposition to elevated LDL-C was associated with presence of aortic valve calcium and incidence of aortic stenosis, providing evidence supportive of a causal association between LDL-C and aortic valve disease. Whether earlier intervention to reduce LDL-C could prevent aortic valve disease merits further investigation.
IMPORTANCE: Plasma low-density lipoprotein cholesterol (LDL-C) has been associated with aortic stenosis in observational studies; however, randomized trials with cholesterol-lowering therapies in individuals with established valve disease have failed to demonstrate reduced disease progression. OBJECTIVE: To evaluate whether genetic data are consistent with an association between LDL-C, high-density lipoprotein cholesterol (HDL-C), or triglycerides (TG) and aortic valve disease. DESIGN, SETTING, AND PARTICIPANTS: Using a Mendelian randomization study design, we evaluated whether weighted genetic risk scores (GRSs), a measure of the genetic predisposition to elevations in plasma lipids, constructed using single-nucleotide polymorphisms identified in genome-wide association studies for plasma lipids, were associated with aortic valve disease. We included community-based cohorts participating in the CHARGE consortium (n = 6942), including the Framingham Heart Study (cohort inception to last follow-up: 1971-2013; n = 1295), Multi-Ethnic Study of Atherosclerosis (2000-2012; n = 2527), Age Gene/Environment Study-Reykjavik (2000-2012; n = 3120), and the Malmö Diet and Cancer Study (MDCS, 1991-2010; n = 28,461). MAIN OUTCOMES AND MEASURES: Aortic valve calcium quantified by computed tomography in CHARGE and incident aortic stenosis in the MDCS. RESULTS: The prevalence of aortic valve calcium across the 3 CHARGE cohorts was 32% (n = 2245). In the MDCS, over a median follow-up time of 16.1 years, aortic stenosis developed in 17 per 1000 participants (n = 473) and aortic valve replacement for aortic stenosis occurred in 7 per 1000 (n = 205). Plasma LDL-C, but not HDL-C or TG, was significantly associated with incident aortic stenosis (hazard ratio [HR] per mmol/L, 1.28; 95% CI, 1.04-1.57; P = .02; aortic stenosis incidence: 1.3% and 2.4% in lowest and highest LDL-C quartiles, respectively). The LDL-C GRS, but not HDL-C or TG GRS, was significantly associated with presence of aortic valve calcium in CHARGE (odds ratio [OR] per GRS increment, 1.38; 95% CI, 1.09-1.74; P = .007) and with incident aortic stenosis in MDCS (HR per GRS increment, 2.78; 95% CI, 1.22-6.37; P = .02; aortic stenosis incidence: 1.9% and 2.6% in lowest and highest GRS quartiles, respectively). In sensitivity analyses excluding variants weakly associated with HDL-C or TG, the LDL-C GRS remained associated with aortic valve calcium (P = .03) and aortic stenosis (P = .009). In instrumental variable analysis, LDL-C was associated with an increase in the risk of incident aortic stenosis (HR per mmol/L, 1.51; 95% CI, 1.07-2.14; P = .02). CONCLUSIONS AND RELEVANCE: Genetic predisposition to elevated LDL-C was associated with presence of aortic valve calcium and incidence of aortic stenosis, providing evidence supportive of a causal association between LDL-C and aortic valve disease. Whether earlier intervention to reduce LDL-C could prevent aortic valve disease merits further investigation.
Authors: John E Cosmi; Smadar Kort; Paul A Tunick; Barry P Rosenzweig; Robin S Freedberg; Edward S Katz; Robert M Applebaum; Itzhak Kronzon Journal: Arch Intern Med Date: 2002-11-11
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Authors: Liv J Mundal; Anders Hovland; Jannicke Igland; Marit B Veierød; Kirsten B Holven; Martin Prøven Bogsrud; Grethe S Tell; Trond P Leren; Kjetil Retterstøl Journal: JAMA Cardiol Date: 2019-11-01 Impact factor: 14.676
Authors: Mehdi Afshar; Kevin Luk; Ron Do; Line Dufresne; David S Owens; Tamara B Harris; Gina M Peloso; Kathleen F Kerr; Quenna Wong; Albert V Smith; Mathew J Budoff; Jerome I Rotter; L Adrienne Cupples; Stephen S Rich; James C Engert; Vilmundur Gudnason; Christopher J O'Donnell; Wendy S Post; George Thanassoulis Journal: J Am Coll Cardiol Date: 2017-06-20 Impact factor: 24.094
Authors: Aeron Small; Daniel Kiss; Jay Giri; Saif Anwaruddin; Hasan Siddiqi; Marie Guerraty; Julio A Chirinos; Giovanni Ferrari; Daniel J Rader Journal: Arterioscler Thromb Vasc Biol Date: 2017-02-02 Impact factor: 8.311
Authors: Seamus P Whelton; Andreas C Mauer; Karol M Pencina; Joseph M Massaro; Ralph B D'Agostino; Caroline S Fox; Udo Hoffmann; Erin D Michos; Gina M Peloso; Line Dufresne; James C Engert; Sekar Kathiresan; Matthew Budoff; Wendy S Post; George Thanassoulis; Christopher J O'Donnell Journal: Am J Cardiol Date: 2018-02-13 Impact factor: 2.778
Authors: Emelia J Benjamin; Michael J Blaha; Stephanie E Chiuve; Mary Cushman; Sandeep R Das; Rajat Deo; Sarah D de Ferranti; James Floyd; Myriam Fornage; Cathleen Gillespie; Carmen R Isasi; Monik C Jiménez; Lori Chaffin Jordan; Suzanne E Judd; Daniel Lackland; Judith H Lichtman; Lynda Lisabeth; Simin Liu; Chris T Longenecker; Rachel H Mackey; Kunihiro Matsushita; Dariush Mozaffarian; Michael E Mussolino; Khurram Nasir; Robert W Neumar; Latha Palaniappan; Dilip K Pandey; Ravi R Thiagarajan; Mathew J Reeves; Matthew Ritchey; Carlos J Rodriguez; Gregory A Roth; Wayne D Rosamond; Comilla Sasson; Amytis Towfighi; Connie W Tsao; Melanie B Turner; Salim S Virani; Jenifer H Voeks; Joshua Z Willey; John T Wilkins; Jason Hy Wu; Heather M Alger; Sally S Wong; Paul Muntner Journal: Circulation Date: 2017-01-25 Impact factor: 29.690
Authors: Teresa Trenkwalder; Christopher P Nelson; Muntaser D Musameh; Ify R Mordi; Thorsten Kessler; Costanza Pellegrini; Radoslaw Debiec; Tobias Rheude; Viktor Lazovic; Lingyao Zeng; Andreas Martinsson; J Gustav Smith; Jesper R Gådin; Anders Franco-Cereceda; Per Eriksson; Jonas B Nielsen; Sarah E Graham; Cristen J Willer; Kristian Hveem; Adnan Kastrati; Peter S Braund; Colin N A Palmer; Amparo Aracil; Oliver Husser; Wolfgang Koenig; Heribert Schunkert; Chim C Lang; Christian Hengstenberg; Nilesh J Samani Journal: Int J Cardiol Date: 2018-11-17 Impact factor: 4.164