Predictive Utility of Polygenic Risk Scores for Coronary Heart Disease in Three Major Racial and Ethnic Groups

Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African ancestry (AA) and Hispanic ethnicity (HE) individuals is unclear. We investigated associations of "restricted" and genome-wide PRSs with C...

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Veröffentlicht in:	American journal of human genetics Jg. 106; H. 5; S. 707
Hauptverfasser:	Dikilitas, Ozan, Schaid, Daniel J, Kosel, Matthew L, Carroll, Robert J, Chute, Christopher G, Denny, Joshua A, Fedotov, Alex, Feng, QiPing, Hakonarson, Hakon, Jarvik, Gail P, Lee, Ming Ta Michael, Pacheco, Jennifer A, Rowley, Robb, Sleiman, Patrick M, Stein, C Michael, Sturm, Amy C, Wei, Wei-Qi, Wiesner, Georgia L, Williams, Marc S, Zhang, Yanfei, Manolio, Teri A, Kullo, Iftikhar J
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States 07.05.2020
Schlagworte:	coronary artery disease risk prediction hispanic ischemic heart disease coronary heart disease multiethnic genome-wide polygenic score African American polygenic risk scores
ISSN:	1537-6605, 1537-6605
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Abstract	Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African ancestry (AA) and Hispanic ethnicity (HE) individuals is unclear. We investigated associations of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in the U.S. The eMERGE cohort (mean age 48 ± 14 years, 58% female) included 45,645 EA, 7,597 AA, and 2,493 HE individuals. We assessed two restricted PRSs (PRS and PRS ; 28 and 50 variants, respectively) and two genome-wide PRSs (PRS and PRS ; 1.7 M and 6.6 M variants, respectively) derived from EA cohorts. Over a median follow-up of 11.1 years, 2,652 incident CHD events occurred. Hazard and odds ratios for the association of PRSs with CHD were similar in EA and HE cohorts but lower in AA cohorts. Genome-wide PRSs were more strongly associated with CHD than restricted PRSs were. PRS , the best performing PRS, was associated with CHD in all three cohorts; hazard ratios (95% CI) per 1 SD increase were 1.53 (1.46-1.60), 1.53 (1.23-1.90), and 1.27 (1.13-1.43) for incident CHD in EA, HE, and AA individuals, respectively. The hazard ratios were comparable in the EA and HE cohorts (p = 0.77) but were significantly attenuated in AA individuals (p = 2.9 × 10 ). These results highlight the potential clinical utility of PRSs for CHD as well as the need to assemble diverse cohorts to generate ancestry- and ethnicity PRSs.
AbstractList	Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African ancestry (AA) and Hispanic ethnicity (HE) individuals is unclear. We investigated associations of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in the U.S. The eMERGE cohort (mean age 48 ± 14 years, 58% female) included 45,645 EA, 7,597 AA, and 2,493 HE individuals. We assessed two restricted PRSs (PRS and PRS ; 28 and 50 variants, respectively) and two genome-wide PRSs (PRS and PRS ; 1.7 M and 6.6 M variants, respectively) derived from EA cohorts. Over a median follow-up of 11.1 years, 2,652 incident CHD events occurred. Hazard and odds ratios for the association of PRSs with CHD were similar in EA and HE cohorts but lower in AA cohorts. Genome-wide PRSs were more strongly associated with CHD than restricted PRSs were. PRS , the best performing PRS, was associated with CHD in all three cohorts; hazard ratios (95% CI) per 1 SD increase were 1.53 (1.46-1.60), 1.53 (1.23-1.90), and 1.27 (1.13-1.43) for incident CHD in EA, HE, and AA individuals, respectively. The hazard ratios were comparable in the EA and HE cohorts (p = 0.77) but were significantly attenuated in AA individuals (p = 2.9 × 10 ). These results highlight the potential clinical utility of PRSs for CHD as well as the need to assemble diverse cohorts to generate ancestry- and ethnicity PRSs. Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African ancestry (AA) and Hispanic ethnicity (HE) individuals is unclear. We investigated associations of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in the U.S. The eMERGE cohort (mean age 48 ± 14 years, 58% female) included 45,645 EA, 7,597 AA, and 2,493 HE individuals. We assessed two restricted PRSs (PRSTikkanen and PRSTada; 28 and 50 variants, respectively) and two genome-wide PRSs (PRSmetaGRS and PRSLDPred; 1.7 M and 6.6 M variants, respectively) derived from EA cohorts. Over a median follow-up of 11.1 years, 2,652 incident CHD events occurred. Hazard and odds ratios for the association of PRSs with CHD were similar in EA and HE cohorts but lower in AA cohorts. Genome-wide PRSs were more strongly associated with CHD than restricted PRSs were. PRSmetaGRS, the best performing PRS, was associated with CHD in all three cohorts; hazard ratios (95% CI) per 1 SD increase were 1.53 (1.46-1.60), 1.53 (1.23-1.90), and 1.27 (1.13-1.43) for incident CHD in EA, HE, and AA individuals, respectively. The hazard ratios were comparable in the EA and HE cohorts (pinteraction = 0.77) but were significantly attenuated in AA individuals (pinteraction= 2.9 × 10-3). These results highlight the potential clinical utility of PRSs for CHD as well as the need to assemble diverse cohorts to generate ancestry- and ethnicity PRSs.Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African ancestry (AA) and Hispanic ethnicity (HE) individuals is unclear. We investigated associations of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in the U.S. The eMERGE cohort (mean age 48 ± 14 years, 58% female) included 45,645 EA, 7,597 AA, and 2,493 HE individuals. We assessed two restricted PRSs (PRSTikkanen and PRSTada; 28 and 50 variants, respectively) and two genome-wide PRSs (PRSmetaGRS and PRSLDPred; 1.7 M and 6.6 M variants, respectively) derived from EA cohorts. Over a median follow-up of 11.1 years, 2,652 incident CHD events occurred. Hazard and odds ratios for the association of PRSs with CHD were similar in EA and HE cohorts but lower in AA cohorts. Genome-wide PRSs were more strongly associated with CHD than restricted PRSs were. PRSmetaGRS, the best performing PRS, was associated with CHD in all three cohorts; hazard ratios (95% CI) per 1 SD increase were 1.53 (1.46-1.60), 1.53 (1.23-1.90), and 1.27 (1.13-1.43) for incident CHD in EA, HE, and AA individuals, respectively. The hazard ratios were comparable in the EA and HE cohorts (pinteraction = 0.77) but were significantly attenuated in AA individuals (pinteraction= 2.9 × 10-3). These results highlight the potential clinical utility of PRSs for CHD as well as the need to assemble diverse cohorts to generate ancestry- and ethnicity PRSs.
Author	Carroll, Robert J Williams, Marc S Manolio, Teri A Wiesner, Georgia L Dikilitas, Ozan Pacheco, Jennifer A Chute, Christopher G Stein, C Michael Kullo, Iftikhar J Rowley, Robb Wei, Wei-Qi Lee, Ming Ta Michael Fedotov, Alex Feng, QiPing Hakonarson, Hakon Jarvik, Gail P Sleiman, Patrick M Sturm, Amy C Denny, Joshua A Zhang, Yanfei Schaid, Daniel J Kosel, Matthew L
Author_xml	– sequence: 1 givenname: Ozan surname: Dikilitas fullname: Dikilitas, Ozan organization: Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, USA – sequence: 2 givenname: Daniel J surname: Schaid fullname: Schaid, Daniel J organization: Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA – sequence: 3 givenname: Matthew L surname: Kosel fullname: Kosel, Matthew L organization: Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA – sequence: 4 givenname: Robert J surname: Carroll fullname: Carroll, Robert J organization: Department of Biomedical Informatics, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 5 givenname: Christopher G surname: Chute fullname: Chute, Christopher G organization: Schools of Medicine, Public Health, and Nursing, Johns Hopkins University, Baltimore, MD 21205, USA – sequence: 6 givenname: Joshua A surname: Denny fullname: Denny, Joshua A organization: Department of Biomedical Informatics, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 7 givenname: Alex surname: Fedotov fullname: Fedotov, Alex organization: Irving Institute for Clinical and Translational Research, Columbia University Medical Center, New York, NY 10032, USA – sequence: 8 givenname: QiPing surname: Feng fullname: Feng, QiPing organization: Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 9 givenname: Hakon surname: Hakonarson fullname: Hakonarson, Hakon organization: Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA – sequence: 10 givenname: Gail P surname: Jarvik fullname: Jarvik, Gail P organization: Department of Medicine, University of Washington, Seattle, WA 98195, USA – sequence: 11 givenname: Ming Ta Michael surname: Lee fullname: Lee, Ming Ta Michael organization: Geisinger, Danville, PA 17822, USA – sequence: 12 givenname: Jennifer A surname: Pacheco fullname: Pacheco, Jennifer A organization: Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA – sequence: 13 givenname: Robb surname: Rowley fullname: Rowley, Robb organization: National Human Genome Research Institute, Bethesda, MD 20892, USA – sequence: 14 givenname: Patrick M surname: Sleiman fullname: Sleiman, Patrick M organization: Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA – sequence: 15 givenname: C Michael surname: Stein fullname: Stein, C Michael organization: Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 16 givenname: Amy C surname: Sturm fullname: Sturm, Amy C organization: Geisinger, Danville, PA 17822, USA – sequence: 17 givenname: Wei-Qi surname: Wei fullname: Wei, Wei-Qi organization: Department of Biomedical Informatics, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 18 givenname: Georgia L surname: Wiesner fullname: Wiesner, Georgia L organization: Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37212, USA – sequence: 19 givenname: Marc S surname: Williams fullname: Williams, Marc S organization: Geisinger, Danville, PA 17822, USA – sequence: 20 givenname: Yanfei surname: Zhang fullname: Zhang, Yanfei organization: Geisinger, Danville, PA 17822, USA – sequence: 21 givenname: Teri A surname: Manolio fullname: Manolio, Teri A organization: National Human Genome Research Institute, Bethesda, MD 20892, USA – sequence: 22 givenname: Iftikhar J surname: Kullo fullname: Kullo, Iftikhar J email: kullo.iftikhar@mayo.edu organization: Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: kullo.iftikhar@mayo.edu
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Keywords	coronary artery disease risk prediction hispanic ischemic heart disease coronary heart disease multiethnic genome-wide polygenic score African American polygenic risk scores
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Snippet	Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from mainly European ancestry (EA) cohorts, their validity in African...
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Title	Predictive Utility of Polygenic Risk Scores for Coronary Heart Disease in Three Major Racial and Ethnic Groups
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