Type 2 Diabetes Modifies the Association of CAD Genomic Risk Variants With Subclinical Atherosclerosis-Reference-Cited by-同舟云学术

Type 2 Diabetes Modifies the Association of CAD Genomic Risk Variants With Subclinical Atherosclerosis

Published:2023-12 Issue:6 Volume:16 Page:
ISSN:2574-8300
Container-title:Circulation: Genomic and Precision Medicine
language:en
Short-container-title:Circ: Genomic and Precision Medicine

Author:

Hasbani Natalie R.¹,Westerman Kenneth E.²³⁴^ORCID,Kwak Soo Heon⁵,Chen Han¹⁶^ORCID,Li Xihao⁷^ORCID,Di Corpo Daniel⁸,Wessel Jennifer⁹^ORCID,Bis Joshua C.¹⁰^ORCID,Sarnowski Chloè¹,Wu Peitao⁸,Bielak Lawrence F.⁴^ORCID,Guo Xiuqing¹¹^ORCID,Heard-Costa Nancy¹²^ORCID,Kinney Gregory L.¹³^ORCID,Mahaney Michael C.¹⁴^ORCID,Montasser May E.¹⁵^ORCID,Palmer Nicholette D.¹⁶,Raffield Laura M.¹⁷,Terry James G.¹⁸^ORCID,Yanek Lisa R.¹⁹^ORCID,Bon Jessica²⁰^ORCID,Bowden Donald W.¹⁶,Brody Jennifer A.¹⁰^ORCID,Duggirala Ravindranath²¹,Jacobs David R.^ORCID,Kalyani Rita R.¹⁹,Lange Leslie A.²²,Mitchell Braxton D.¹⁵²³^ORCID,Smith Jennifer A.²⁴²⁵^ORCID,Taylor Kent D.¹¹^ORCID,Carson April P.²⁶^ORCID,Curran Joanne E.¹⁴^ORCID,Fornage Myriam²⁷^ORCID,Freedman Barry I.²⁸^ORCID,Gabriel Stacey²⁹,Gibbs Richard A.³⁰,Gupta Namrata²⁹^ORCID,Kardia Sharon L.R.²⁴,Kral Brian G.¹⁹^ORCID,Momin Zeineen³⁰^ORCID,Newman Anne B.³¹^ORCID,Post Wendy S.³²^ORCID,Viaud-Martinez Karine A.³³,Young Kendra A.¹³,Becker Lewis C.¹⁹^ORCID,Bertoni Alain G.³⁴^ORCID,Blangero John¹⁴^ORCID,Carr John J.¹⁸,Pratte Katherine³⁵,Psaty Bruce M.¹⁰³⁶³⁷^ORCID,Rich Stephen S.^ORCID,Wu Joseph C.³⁸³⁹^ORCID,Malhotra Rajeev⁴⁰⁴¹^ORCID,Peyser Patricia A.²⁴^ORCID,Morrison Alanna C.¹^ORCID,Vasan Ramachandran S.¹²⁴²^ORCID,Lin Xihong⁷^ORCID,Rotter Jerome I.^ORCID,Meigs James B.⁴³³⁴,Manning Alisa K.²³⁴^ORCID,de Vries Paul S.¹^ORCID,

Affiliation:

1. Department of Epidemiology Human Genetics and Environmental Sciences, Human Genetics Center, The University of Texas Health Science Center at Houston School of Public Health (N.R.H., H.C., C.S., A.C.M., P.S.d.V.).

2. Department of Medicine, Clinical and Translation Epidemiology Unit (K.E.W., A.K.M.), Massachusetts General Hospital, Boston.

3. Programs in Metabolism and Medical and Population Genetics (K.E.W., J.B.M., A.K.M.), Broad Institute, Cambridge.

4. Department of Medicine, Harvard Medical School, Boston, MA (K.E.W., J.B.M., A.K.M.).

5. Department of Internal Medicine, Seoul National University Hospital, South Korea (S.H.K.).

6. School of Biomedical Informatics, Center for Precision Health (H.C.), The University of Texas Health Science Center at Houston.

7. Department of Biostatistics, Harvard T.H. Chan School of Public Health (X. Li, X. Lin), Boston University School of Public Health, MA.

8. Department of Biostatistics (D.D., P.W.), Boston University School of Public Health, MA.

9. Department of Epidemiology, Fairbanks School of Public Health, Indianapolis, IN (J.W.).

10. Department of Medicine, Cardiovascular Health Research Unit (J.C.B., J.A.B., B.M.P.), University of Washington, Seattle.

11. Department of Pediatrics, The Institute for Translational Genomics and Population Sciences, The Lundquist Institute for Biomedical Innovation at Harbor-University of California Los Angeles Medical Center, Torrance (X.G., K.D.T.).

12. Framingham Heart Study, MA (N.H.-C., R.S.V.).

13. Department of Epidemiology, University of Colorado School of Public Health, Aurora (G.L.K., K.A.Y.).

14. Department of Human Genetics and South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley School of Medicine, Brownsville (M.C.M., J.E.C., J. Blangero).

15. Department of Medicine, Division of Endocrinology Diabetes and Nutrition, University of Maryland School of Medicine, Baltimore (M.E.M., B.D.M.).

16. Department of Biochemistry (N.D.P., D.W.B.), Wake Forest School of Medicine, Winston-Salem, NC.

17. Department of Genetics, University of North Carolina at Chapel Hill (L.M.R.).

18. Department of Radiology, Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University Medical Center, Nashville, TN (J.G.T., J.J.C.).

19. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD (L.R.Y., R.R.K., B.G.K., L.C.B.).

20. Department of Medicine, Division of Pulmonary Allergy and Critical Care Medicine, University of Pittsburgh Medical Center, PA (J. Bon).

21. Department of Human Genetics and South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley School of Medicine, McAllen (R.D.).

22. Division of Biomedical Informatics and Personalized Medicine, School of Medicine University of Colorado, Aurora (L.A.L.).

23. Geriatrics Research and Education Clinical Center, Baltimore Veterans Administration Medical Center, MD (B.D.M.).

24. Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor (L.F.B., J.A.S., S.L.R.K., P.A.P.).

25. Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor (J.A.S.).

26. Department of Medicine, University of Mississippi Medical Center, Jackson (A.P.C.).

27. Institute of Molecular Medicine (M.F.), The University of Texas Health Science Center at Houston.

28. Department of Internal Medicine, Section on Nephrology (B.I.F.), Wake Forest School of Medicine, Winston-Salem, NC.

29. Genomics Platform (S.G., N.G.), Broad Institute, Cambridge.

30. Baylor College of Medicine Human Genome Sequencing Center, Houston, TX (R.A.G., Z.M.).

31. Department of Epidemiology, University of Pittsburgh School of Public Health, PA (A.B.N.).

32. Division of Cardiology, Johns Hopkins Medicine, Baltimore, MD (W.S.P.).

33. Illumina Laboratory Services, Illumina, Inc, San Diego, CA (K.A.V.-M.).

34. Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, NC (A.G.B.).

35. Department of Biostatistics, National Jewish Health, Denver, CO (K.P.).

36. Department of Epidemiology (B.M.P.), University of Washington, Seattle.

37. Department of Health Systems and Population Health (B.M.P.), University of Washington, Seattle.

38. Center for Public Health Genomics, University of Virginia School of Medicine, Charlottesville (J.C.W.).

39. Department of Medicine, Division of Cardiovascular Medicine, Stanford Cardiovascular Institute, Stanford University School of Medicine (J.C.W.), Stanford University, CA.

40. Division of Cardiology (R.M.), Massachusetts General Hospital, Boston.

41. Department of Radiology Molecular Imaging Program at Stanford (R.M.), Stanford University, CA.

42. Department of Quantitative and Qualitative Health Sciences, University of Texas Health San Antonio School of Public Health (R.S.V.).

43. Division of General Internal Medicine (J.B.M.), Massachusetts General Hospital, Boston.

Abstract

BACKGROUND: Individuals with type 2 diabetes (T2D) have an increased risk of coronary artery disease (CAD), but questions remain about the underlying pathology. Identifying which CAD loci are modified by T2D in the development of subclinical atherosclerosis (coronary artery calcification [CAC], carotid intima-media thickness, or carotid plaque) may improve our understanding of the mechanisms leading to the increased CAD in T2D. METHODS: We compared the common and rare variant associations of known CAD loci from the literature on CAC, carotid intima-media thickness, and carotid plaque in up to 29 670 participants, including up to 24 157 normoglycemic controls and 5513 T2D cases leveraging whole-genome sequencing data from the Trans-Omics for Precision Medicine program. We included first-order T2D interaction terms in each model to determine whether CAD loci were modified by T2D. The genetic main and interaction effects were assessed using a joint test to determine whether a CAD variant, or gene-based rare variant set, was associated with the respective subclinical atherosclerosis measures and then further determined whether these loci had a significant interaction test. RESULTS: Using a Bonferroni-corrected significance threshold of P <1.6×10 −4 , we identified 3 genes ( ATP1B1 , ARVCF , and LIPG ) associated with CAC and 2 genes ( ABCG8 and EIF2B2 ) associated with carotid intima-media thickness and carotid plaque, respectively, through gene-based rare variant set analysis. Both ATP1B1 and ARVCF also had significantly different associations for CAC in T2D cases versus controls. No significant interaction tests were identified through the candidate single-variant analysis. CONCLUSIONS: These results highlight T2D as an important modifier of rare variant associations in CAD loci with CAC.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

General Medicine

Reference41 articles.

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4. Genetics Insights in the Relationship Between Type 2 Diabetes and Coronary Heart Disease

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