Polygenic Hyperlipidemias and Coronary Artery Disease Risk
Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LD...
Gespeichert in:
| Veröffentlicht in: | Circulation. Genomic and precision medicine Jg. 13; H. 2; S. e002725 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
01.04.2020
|
| Schlagworte: | |
| ISSN: | 2574-8300, 2574-8300 |
| Online-Zugang: | Weitere Angaben |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| Abstract | Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk.
We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen).
In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82-2.94) to 3.78 (95% CI, 3.71-3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18-1.20) mmol/L, ranging from 0.97 (95% CI, 0.94-1.00) to 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).
The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation. |
|---|---|
| AbstractList | Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk.
We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen).
In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82-2.94) to 3.78 (95% CI, 3.71-3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18-1.20) mmol/L, ranging from 0.97 (95% CI, 0.94-1.00) to 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).
The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation. Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk.BACKGROUNDHyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk.We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen).METHODSWe derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen).In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82-2.94) to 3.78 (95% CI, 3.71-3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18-1.20) mmol/L, ranging from 0.97 (95% CI, 0.94-1.00) to 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).RESULTSIn FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82-2.94) to 3.78 (95% CI, 3.71-3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18-1.20) mmol/L, ranging from 0.97 (95% CI, 0.94-1.00) to 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation.CONCLUSIONSThe CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation. |
| Author | Benner, Christian Lin, Jake Rämö, Joel T Kiiskinen, Tuomo Fu, Yu Freimer, Nelson B Pirinen, Matti Ripatti, Pietari Ripatti, Samuli Palotie, Aarno Söderlund, Sanni Havulinna, Aki S Palta, Priit Widén, Elisabeth Taskinen, Marja-Riitta Mars, Nina J Surakka, Ida Tukiainen, Taru Salomaa, Veikko |
| Author_xml | – sequence: 1 givenname: Pietari surname: Ripatti fullname: Ripatti, Pietari organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 2 givenname: Joel T surname: Rämö fullname: Rämö, Joel T organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 3 givenname: Nina J surname: Mars fullname: Mars, Nina J organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 4 givenname: Yu surname: Fu fullname: Fu, Yu organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 5 givenname: Jake surname: Lin fullname: Lin, Jake organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 6 givenname: Sanni surname: Söderlund fullname: Söderlund, Sanni organization: Department of Internal Medicine, Helsinki University Hospital, Helsinki, Finland (S.S.) – sequence: 7 givenname: Christian surname: Benner fullname: Benner, Christian organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 8 givenname: Ida surname: Surakka fullname: Surakka, Ida organization: Department of Internal Medicine, University of Michigan, Ann Arbor, MI (I.S.) – sequence: 9 givenname: Tuomo surname: Kiiskinen fullname: Kiiskinen, Tuomo organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 10 givenname: Aki S surname: Havulinna fullname: Havulinna, Aki S organization: Department of Public Health Solutions, Finnish Institute for Health and Welfare, Helsinki, Finland (A.S.H., V.S.) – sequence: 11 givenname: Priit surname: Palta fullname: Palta, Priit organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 12 givenname: Nelson B surname: Freimer fullname: Freimer, Nelson B organization: Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behaviour, University of California, Los Angeles, CA (N.B.F.) – sequence: 13 givenname: Elisabeth surname: Widén fullname: Widén, Elisabeth organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 14 givenname: Veikko surname: Salomaa fullname: Salomaa, Veikko organization: Department of Public Health Solutions, Finnish Institute for Health and Welfare, Helsinki, Finland (A.S.H., V.S.) – sequence: 15 givenname: Taru surname: Tukiainen fullname: Tukiainen, Taru organization: Institute for Molecular Medicine Finland, Helsinki Institute of Life Science (HiLIFE) (P.R., J.T.R., N.J.M., Y.F., J.L., C.B., I.S., T.K., A.S.H., P.P., E.W., T.T., M.P., A.P., S.R.), University of Helsinki, Helsinki, Finland – sequence: 16 givenname: Matti surname: Pirinen fullname: Pirinen, Matti organization: Department of Mathematics and Statistics, Faculty of Science (M.P.), University of Helsinki, Helsinki, Finland – sequence: 17 givenname: Aarno surname: Palotie fullname: Palotie, Aarno organization: Department of Neurology (A.P.), Massachusetts General Hospital, Boston, MA – sequence: 18 givenname: Marja-Riitta surname: Taskinen fullname: Taskinen, Marja-Riitta organization: Clinical Research Institute HUCH, Ltd, Helsinki, Finland (M.-R.T.) – sequence: 19 givenname: Samuli surname: Ripatti fullname: Ripatti, Samuli organization: Broad Institute of MIT and Harvard, Cambridge, MA (S.R.) |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32154731$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNj01Lw0AQhhep2Fr7BzxIjl5SZ7-yWW8lrW2hqJTewyY7kdV8mW0O-fcGrODpmYHnHea9JZO6qZGQewpLSiP6lOyPyXbzOi56CcAUk1dkxqQSYcwBJv_mKVl4_wkAVGsdseiGTDmjUihOZ-T5vSmHD6xdHuyGFrvStc5i5YwPTG2DpOma2nRDsOrOOGLtPBqPwdH5rztyXZjS4-LCOTm9bE7JLjy8bffJ6hDmknIeagOZFhKsRBMVphDKZlER55bGhUIwNlNgdSYktVyNmhKi0CLWPIdcZZbNyePv2bZrvnv057RyPseyNDU2vU_ZmIojpgSM6sNF7bMKbdp2rhqfT__qsh-cxFnF |
| CitedBy_id | crossref_primary_10_1016_j_jrras_2024_100930 crossref_primary_10_1016_j_crmeth_2022_100166 crossref_primary_10_1016_j_ajhg_2024_06_013 crossref_primary_10_1210_clinem_dgab876 crossref_primary_10_1038_s10038_021_00929_7 crossref_primary_10_1016_j_jrras_2024_100970 crossref_primary_10_1093_toxsci_kfac103 crossref_primary_10_1038_s41569_021_00638_w crossref_primary_10_1038_s41591_022_02122_5 crossref_primary_10_1186_s12916_020_01762_z crossref_primary_10_1186_s13073_021_00994_9 crossref_primary_10_1186_s12916_021_01977_8 crossref_primary_10_3390_biomedicines12040818 crossref_primary_10_1038_s43856_025_00981_w crossref_primary_10_3390_v16071161 crossref_primary_10_1016_j_mmm_2021_12_007 crossref_primary_10_1097_MOL_0000000000000733 crossref_primary_10_1038_s41467_024_46102_4 crossref_primary_10_1161_ATVBAHA_120_315904 crossref_primary_10_1210_endocr_bqae146 crossref_primary_10_1016_j_msard_2021_103255 crossref_primary_10_1186_s12920_021_01127_2 crossref_primary_10_2217_bmm_2022_0797 crossref_primary_10_1097_MOL_0000000000000737 crossref_primary_10_3390_biomedicines12030617 crossref_primary_10_1186_s12920_023_01717_2 crossref_primary_10_3390_genes15050639 crossref_primary_10_1080_14779072_2025_2534707 crossref_primary_10_1038_s41467_021_26277_w crossref_primary_10_3389_fcvm_2022_978998 crossref_primary_10_1177_00033197251350182 crossref_primary_10_1016_j_jacl_2020_11_006 crossref_primary_10_1161_CIRCRESAHA_123_323284 crossref_primary_10_15829_1560_4071_2024_5874 crossref_primary_10_1002_advs_202405955 crossref_primary_10_1007_s00335_023_10017_0 crossref_primary_10_1038_s41588_022_01221_w crossref_primary_10_15829_1728_8800_2023_3846 crossref_primary_10_1186_s13073_021_00831_z crossref_primary_10_1038_s41467_022_33510_7 crossref_primary_10_1038_s41598_025_13411_7 crossref_primary_10_1161_ATVBAHA_125_322801 crossref_primary_10_1371_journal_pgen_1011159 crossref_primary_10_1002_gepi_22392 crossref_primary_10_1210_endocr_bqaf100 crossref_primary_10_1089_met_2023_0125 crossref_primary_10_1093_humrep_deab086 crossref_primary_10_1097_MOL_0000000000000796 crossref_primary_10_3390_nu15204385 crossref_primary_10_1093_hmg_ddaa136 crossref_primary_10_1016_j_atherosclerosis_2023_117384 crossref_primary_10_1002_jbmr_4904 crossref_primary_10_1038_s41598_022_07465_0 crossref_primary_10_1161_ATVBAHA_123_320065 crossref_primary_10_1016_j_jhep_2022_04_010 crossref_primary_10_1097_HCO_0000000000000839 crossref_primary_10_3390_ijms22041593 crossref_primary_10_3390_genes15040462 crossref_primary_10_1016_j_tig_2021_08_009 crossref_primary_10_1093_genetics_iyaf018 |
| ContentType | Journal Article |
| CorporateAuthor | FinnGen |
| CorporateAuthor_xml | – name: FinnGen |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1161/CIRCGEN.119.002725 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 2574-8300 |
| ExternalDocumentID | 32154731 |
| Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: British Heart Foundation grantid: CH/1996001/9454 – fundername: Medical Research Council grantid: MC_PC_17228 – fundername: Medical Research Council grantid: MC_QA137853 |
| GroupedDBID | 53G AAAAV AAHPQ AAIQE AAJCS AASCR ABASU ABDIG ABJNI ABPXF ABVCZ ABXYN ABZZY ACEWG ACILI ACXJB ADGGA ADHPY AEBDS AFBFQ AFDTB AFEXH AFNMH AHQNM AHQVU AHVBC AINUH AJCLO AJIOK AJNWD AJZMW AKCTQ ALKUP ALMA_UNASSIGNED_HOLDINGS ALMTX AMJPA AMKUR AMNEI AOHHW AOQMC BQLVK C45 CGR CUY CVF DIWNM EBS ECM EEVPB EIF EJD FCALG GNXGY GQDEL HLJTE IKREB IPNFZ KQB NPM ODMTH ODZKP OHYEH OPUJH OVD OVDNE OXXIT RAH RIG RLZ TEORI TSPGW W2D 7X8 ADKSD |
| ID | FETCH-LOGICAL-c5133-9a0b9450d5ea6faf47db6f8cd18f7e0adb70d9b451d3750d744f94893c0c7bd2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 71 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000529978000004&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 2574-8300 |
| IngestDate | Thu Oct 02 10:42:03 EDT 2025 Sat May 31 02:11:21 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | coronary artery disease hypertriglyceridemia risk factors humans hypercholesterolemia |
| Language | English |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c5133-9a0b9450d5ea6faf47db6f8cd18f7e0adb70d9b451d3750d744f94893c0c7bd2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://www.ahajournals.org/doi/pdf/10.1161/CIRCGEN.119.002725 |
| PMID | 32154731 |
| PQID | 2375862740 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_2375862740 pubmed_primary_32154731 |
| PublicationCentury | 2000 |
| PublicationDate | 2020-April-01 |
| PublicationDateYYYYMMDD | 2020-04-01 |
| PublicationDate_xml | – month: 04 year: 2020 text: 2020-April-01 day: 01 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Circulation. Genomic and precision medicine |
| PublicationTitleAlternate | Circ Genom Precis Med |
| PublicationYear | 2020 |
| SSID | ssj0001999626 |
| Score | 2.4048295 |
| Snippet | Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | e002725 |
| SubjectTerms | Cholesterol, LDL - blood Cohort Studies Coronary Artery Disease - blood Coronary Artery Disease - epidemiology Coronary Artery Disease - etiology Female Genetic Predisposition to Disease Genome-Wide Association Study Humans Hyperlipidemias - complications Hyperlipidemias - genetics Male Middle Aged Multifactorial Inheritance Polymorphism, Single Nucleotide Prognosis Risk Factors Triglycerides - blood |
| Title | Polygenic Hyperlipidemias and Coronary Artery Disease Risk |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/32154731 https://www.proquest.com/docview/2375862740 |
| Volume | 13 |
| WOSCitedRecordID | wos000529978000004&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1JS8NAFB7UinhxX-pGBK_BSWaSyXgRia0VbCilh97CZBYIlqQ2KvTf-yZJ6UkQvCTkkDC8fHn53jLvQ-iOcgNu3_iuVoK4VBLicqoVRK1MUUaEYaaeM_vGkiSaTvmoTbhVbVvlyifWjlqV0ubI730CzNYKxeDH-YdrVaNsdbWV0NhEHQJUxrZ0sWm0zrFYNl8rrgEwqRsRjFf7ZkLvPn4dxy-9BC7syEqf-cHvLLP-2_T3_7vOA7TX8kznqQHGIdrQxRHaGbaV9GP0MCpnSwBPLp0BhKKLWd5IxYrKEYVyYjvYQCyW9gEaTs9NHccZ59X7CZr0e5N44LY6Cq606i0uFzjjNMAq0CI0wlBm995FUnmRYRoLlTGseEYDT8HisWKUGm6H0kgsWab8U7RVlIU-R06kwIQ6CjmQCup7RnBNPSqEVoR4Mgi76HZllBRgamsPotDlV5WuzdJFZ41l03kzTyMlQDsAF97FH-6-RLu-jXjr3pkr1DHwkeprtC2_P_NqcVO_fzgmo-EPLcu4jA |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Polygenic+Hyperlipidemias+and+Coronary+Artery+Disease+Risk&rft.jtitle=Circulation.+Genomic+and+precision+medicine&rft.au=Ripatti%2C+Pietari&rft.au=R%C3%A4m%C3%B6%2C+Joel+T&rft.au=Mars%2C+Nina+J&rft.au=Fu%2C+Yu&rft.date=2020-04-01&rft.eissn=2574-8300&rft.volume=13&rft.issue=2&rft.spage=e002725&rft_id=info:doi/10.1161%2FCIRCGEN.119.002725&rft_id=info%3Apmid%2F32154731&rft_id=info%3Apmid%2F32154731&rft.externalDocID=32154731 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2574-8300&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2574-8300&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2574-8300&client=summon |